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Microbial Cell, Vol. 2, No. 4, pp. 94 - 104; DOI: 10.15698/mic2015.04.198
Translate to divide: сontrol of the cell cycle by protein synthesis
1 Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA.
2 Department of Biology, Texas A&M University, College Station, TX 77843, USA.
Keywords: protein synthesis, ribosome biogenesis, ribosome profiling, START, translational control.
Received: 20/01/2015 Accepted: 07/03/2015 Published: 20/03/2015
Michael Polymenis, Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA, email@example.com
Rodolfo Aramayo, Department of Biology, Texas A&M University, College Station, TX 77843, USA, firstname.lastname@example.org
Conflict of interest statement: The authors declare no conflict of interest.
Please cite this article as: Michael Polymenis and Rodolfo Aramayo (2015). Translate to divide: Control of the cell cycle by protein synthesis. Microbial Cell 2(4): 94-104.
Protein synthesis underpins much of cell growth and, consequently, cell multiplication. Understanding how proliferating cells commit and progress into the cell cycle requires knowing not only which proteins need to be synthesized, but also what determines their rate of synthesis during cell division.
Experiments with proliferating populations of microbial strains, animal or plant cell lines, have rigorous expectations. Under the same culture conditions, cells ought to have the same properties and composition in every single experiment. The basic “metrics” of proliferating cells remain constant, even after many rounds of cell division . These metrics include cellular mass and volume, and macromolecular composition . The constancy of such parameters reflects the fundamental ability of cells to coordinate their growth with their division . Balancing cell growth with cell division determines the overall rates of cell proliferation . Despite the obvious significance of this phenomenon, how cells manage to coordinate their growth with their division remains largely mysterious.
Proteins are often the most abundant macromolecules in proliferating cells. For example, in steady-state cultures of the budding yeast Saccharomyces cerevisiae, the protein content ranges from 35% to 44% of all macromolecules, depending on culture conditions . Furthermore, much of the proteome (>20%) is dedicated to making ribosomes and translation factors, enabling cells to make more proteins . On top of that, making ribosomal components and assembling them into functional ribosomes involves a dizzying array of molecular players and cellular processes . Consequently, protein synthesis is viewed as a fundamental measure of cell growth. Decades ago, a founding father of cell cycle studies put it this way: “No sensible interpretation of cell growth can be made without a knowledge of the overall pattern of protein synthesis” .
In the following sections, we discuss the interplay of protein synthesis and cell division. Examples of translational control in embryonic and meiotic cell divisions have been covered comprehensively elsewhere . Here, the focus is on mitotic cell division and specifically on the G1 phase of the cell cycle, when cells commit to a new round of cell division. The examples discussed are mainly, but not exclusively, from the budding yeast S. cerevisiae. The discussion centers on un-perturbed, continuously dividing cells, and the impact of genetic, nutritional or chemical perturbations.
FIGURE 1: Schematic overview of the topics covered in this review.
Open reading frames (ORFs) are shown in red.
OVERALL PATTERN OF PROTEIN SYNTHESIS IN THE CELL CYCLE
In animal cells, protein synthesis is much lower in mitosis than in other cell cycle phases . Mechanisms that enable translation of specific mRNAs in animal cells undergoing mitosis have been reviewed elsewhere . In contrast to the mitotic block in protein synthesis in animal cells, early studies indicated that budding yeast cells synthesize proteins, including ribosomal proteins, continuously during the cell cycle . These experiments relied mostly on incorporation of labeled amino acids into polypeptides, which were then visualized after electrophoresis . Hence, those early experiments sampled abundant, constitutively expressed proteins that make up the vast majority of the proteome . Obviously, transcriptional waves drive periodic synthesis of hundreds of proteins in the cell cycle . Nonetheless, the bulk of cellular protein synthesis appears to proceed at an exponentially increasing rate in the cell cycle . This conclusion was reinforced by monitoring the accumulation of constitutively expressed fluorescent proteins in single cells . In addition, continuous monitoring of cell volume supports an exponential mode of increase in the cell cycle . Therefore, it appears that budding yeast cells make proteins and grow exponentially. Based on buoyant mass as a metric of cell growth, the same can be said about the growth of diverse types of cells, from bacteria to mouse lymphoblasts, with heavier cells growing faster than lighter cells . However, whether or not the growth of animal cells is exponential is still controversial .
An exponential mode of protein synthesis and growth is consistent with the existence of active mechanisms that sense some growth metric, perhaps somehow related to protein synthesis . Such mechanisms would enable cells to monitor their growth and commit to a new round of cell division once their growth requirements are met . As a result, cells that are born small stay longer in the G1 phase, until they grow enough to commit into and initiate a new round of cell division . In yeast, the point of commitment to a new round of cell division is called START . START is marked molecularly by nuclear eviction of the Whi5p repressor , a protein that functions analogously to the retinoblastoma gene product of animal cells . Once cells pass through START in late G1, they will initiate and complete their division even if they encounter growth limitations . To summarize simply, it seems that the bigger yeast cells get, the faster they make proteins and grow, propelling them to divide. This simple concept raises a series of key questions: What determines the rate of protein synthesis? How can the rate of protein synthesis be altered and what would the effects of such alterations be on the cell cycle? What are the RNA targets of translational control that affect cell cycle progression?
INITIATE TO START?
The rate of synthesis of any given protein depends on not only the concentration but also the translational efficiency of its mRNA. Discrepancies between the two parameters underpin translational control. It is often stated that control of translation in eukaryotic cells is exercised mainly at the initiation step, when ribosomes are recruited to mRNA . As discussed in subsequent sections, additional layers of control may also change the rate at which proteins are made. Nonetheless, the initiation step remains a key control point of translation . Ribosomal recruitment in eukaryotes usually involves recognition of a cap structure at the 5’-end of the mRNA. The small (40S) ribosomal subunit loaded with initiator Met-tRNA and with the contribution of various initiation factors begins scanning the 5’-UTR of the mRNA for an AUG (or near-cognate start codons). In the process, it has to navigate past the secondary structure of the 5’-UTR  or initiation codons upstream of the main open reading frame . Such features may affect recognition and initiation from the correct start codon .
The earliest genetic evidence for specific cell cycle effects due to translational control was the isolation of budding yeast conditional mutants in what turned out to be translation initiation factors . One would expect that cessation of a continuous vital cellular function, such as initiation of translation, would simply arrest each cell at whichever point in the cycle that cell happened to be at the time. In an asynchronously proliferating cell population, this would manifest in a pattern of random arrests along the cell cycle . Yet cell division cycle (cdc) genetic screens yielded mutants carrying temperature-sensitive, hypomorphic alleles of translation initiation factors, which did not display a random arrest at their non-permissive temperature. Instead, cells carrying cdc33 (encoding mRNA cap binding protein and translation initiation factor eIF4E ) or cdc63 (encoding the b subunit of translation initiation factor eIF3 ) mutations arrest uniformly in the G1 phase of the cell cycle, unable to initiate DNA replication and a new round of cell division . A conditional methionyl-tRNA synthetase (mes1) mutant also arrests in the G1 phase of the cell cycle . These classical genetic analyses suggested strongly that G1 transit is sensitive to translation initiation, more so than other phases of the cell cycle. This conclusion was strengthened when essential gene function was interrogated with a collection of titratable TetO7 promoter alleles for essential genes . In addition to the eIF4E and eIF3b examples mentioned above, Yu et al. showed that inhibiting expression of eIF2a, eIF4A, eIF2b, eIF3i, or eIF1 resulted in G1 arrest in yeast (; and Table 1). Hence, impairing translation initiation in a number of ways, invariably and specifically also impairs the capacity of cells to initiate a new round of cell division.
If initiation of translation is important for commitment to division, then signaling pathways that control initiation of division may do so, at least in part, by regulating translation initiation. Mitogenic pathways would be expected to activate translation initiation, while pathways that convey anti-proliferative signals may inhibit translation initiation. The cardinal example for the former case is the Target of Rapamycin (TOR) pathway. How the TOR pathway activates initiation of translation and overall protein synthesis has been reviewed elsewhere . Loss of TOR function was known to cause G1 arrest in mammals  and yeast . Connecting the G1 arrest with the effects of TOR on translation, however, was not obvious. In a landmark paper, it was shown that upon loss of TOR function in yeast, the cause of the G1 arrest was a direct consequence of a block in translation initiation . De-repressing translation of the G1 cyclin Cln3p was sufficient to abrogate the G1 arrest of TOR-inhibited yeast cells . TOR is not the only mitogenic pathway that activates translation initiation. The RAS/MAPK pathway in animals phosphorylates and increases the activity of eIF4B . Remarkably, phosphorylation of eIF4B on the same residue is a common output of both the TOR and MAPK pathways , underscoring the significance of activating translation initiation for commitment to cell division. Conversely, upon stress or starvation it is not prudent to either initiate cell division or make many proteins. It turns out that phosphorylation of eIF2α is a conserved response from yeast to mammals that inhibits overall translation initiation, and it is an output of anti-mitogenic signals .
TABLE 1. Cell cycle phenotypes of loss-of-function mutants in essential genes encoding protein synthesis and ribosome biogenesis factors in S. cerevisiae.
TRANSLATIONAL TARGETS (?) FOR COMMITMENT TO DIVISION
The above examples suggest that translation initiation goes hand-in-hand with G1 progression and initiation of cell division. By and large, however, they do not answer how this is brought about. What are the relevant proteins important for G1 transit, whose synthesis is sensitive to limitations in translation initiation, and how do these proteins impinge on the machinery of cell division? In the case of the G1 cyclin Cln3p was mentioned above, Hall and colleagues replaced the long 5’-UTR of the yeast CLN3 mRNA with that of UBI4, which is efficiently translated when TOR function is low . Cells carrying this non-repressible CLN3 did not arrest in G1 when TOR function was inhibited by rapamycin . Similarly, efficient translation of CLN3 enabled G1 arrested cdc33 cells, in which the activity of the eIF4E is impaired (see Table 1), to initiate cell division . The Whi3p RNA-binding protein, which sequesters CLN3 mRNA in cytoplasmic foci, may inhibit translation of CLN3 . There is also a uORF in the 5’-UTR of the CLN3 mRNA . We had proposed that the uORF lowers the number of scanning ribosomes that reach the downstream main AUG, especially when the ribosome content of the cell is low in poor media . As predicted, inactivation of the uORF in CLN3 allowed cells growing in poor medium, with glycerol as the source for carbon, to accelerate completion of START . Nitrogen limitation was also reported to repress translation of CLN3 . In contrast, another study reported that 20 min after amino acid starvation, translation of CLN3 was up-regulated . While this later discrepancy may simply reflect the different experimental set-ups, there is overall compelling evidence that synthesis of Cln3p, whose levels control the timing of START , is regulated at least in part at the translational level. It should be noted, however, that all the examples above rest on comparisons between different conditions: with or without inhibitors of TOR ; mutant vs. wild type ; different nutrients . It is important to stress that although CLN3 is a translational target, there is no evidence yet that it is targeted in a periodic manner in the cell cycle, in G1 or any other cell cycle phase.
It has been reported that CLN3 transcription oscillates early in the cell cycle , but Cln3p protein levels were not evaluated in these studies. Cln3p is very unstable , and difficult to detect by immunoblotting. Early studies reported that Cln3p levels do not oscillate in the cell cycle . Recently, however, more sensitive approaches from two independent studies showed that Cln3p protein is nearly absent in early G1 cells, but it gradually accumulates as cells approach START (Fig. 9 in , and Fig. 10 in ), without a corresponding increase in the mRNA levels of CLN3. The data from Thorburn et al.  and Zapata et al.  strongly implicate post-transcriptional mechanisms that control abundance of Cln3p in the cell cycle, perhaps due to control of its synthesis, degradation, or both. Both of these studies relied on centrifugal elutriation to isolate highly synchronous early G1 daughter cells, which were then sampled as they progressed in the cell cycle . Until analogous studies are performed with alternative synchronization methods, it is formally possible that the results reflect idiosyncrasies of elutriation. Note also that the CLN3 mRNA cannot possibly be the only physiological target of translational control for cell cycle progression. Cells lacking Cln3p are viable  and they also respond as expected to nutrient limitations, reducing their size .
In other systems, the best example of a translational target important for initiation of mitotic cell division is the cyclin-dependent kinase inhibitor p27Kip1 in human cells, whose translation appears to be periodic in the cell cycle, decreasing at the G1/S transition . Translational control of p27Kip1 is complex, involving both cap-dependent and independent mechanisms . However, because p27Kip1 synthesis decreases at the G1/S transition, this case of translational control cannot account for the postulated activating role of protein synthesis in triggering cell division. Other reported translational targets include the G1 cyclin D1 in mammals , and the G1/S cyclins E1  and E2  in mammals, and Cig2 in fission yeast  (reviewed in ). Trans-acting factors influencing translation initiation of these targets include the helicase DDX3 for cyclin E1  and Ded1 for Cig2 . It is not clear, however, if translation of these cyclins is periodic in cycling cells. Alternatively, their translational regulation may be an output of a continuous process that affects their overall levels. The levels of these cyclins may oscillate in the cell cycle for other reasons, such as mechanisms that control mRNA levels and protein degradation. Overall, there is a critical gap in our understanding of the role of translational control in mitotic cell cycle progression, especially in G1 progression and commitment to division. There have not been any studies that directly and systematically looked for mRNAs that are translated differentially in the G1 phase, in cycling, un-perturbed cells.
START ON CYCLOHEXIMIDE
After the initiation step, the rate of translation depends on the concentration and activity of translating ribosomes that elongate the nascent polypeptides. If elongation of protein synthesis is inhibited, then what are the consequences on cell cycle progression? This question was first tackled pharmacologically, monitoring cell cycle progression in the presence of varying doses of cycloheximide . Cycloheximide inhibits the translocation step in eukaryotic 80S ribosomes, blocking translational elongation . Increasing doses of cycloheximide increase the population doubling time, mostly because cells spend more time in the G1 phase of the cell cycle . Cycloheximide also affects size homeostasis. In budding yeast, cycloheximide reduces the newborn cell size  and the rate at which cells increase in size . It also increases the critical size threshold for START . These changes account for the increase in the duration of the G1 phase upon treatment with cycloheximide. The effects of cycloheximide support the notion that a critical rate of protein synthesis is required for G1 transit and completion of START in budding yeast  and animal cells . The reports that interrogated cycloheximide’s effects on G1 progression have been influential. They have often been taken to imply a requirement for the continuous synthesis of unstable protein(s), whose rate of synthesis parallels overall protein synthesis rates and cell growth. Identifying those proteins and how they affect the cell division machinery would then hold the promise of explaining molecularly how cells couple their growth with their division . Various such candidate proteins have been proposed over the years. However, there is no report of a protein whose levels increase due to cell cycle-dependent translational control, as cycling cells approach START .
RIBOSOME MAKES PROTEIN MAKES CELLS?
Ribosomes are the complex macromolecular machines that catalyze protein synthesis. Hence, changing the concentration of functional ribosomes in the cell is expected to change the overall rates of protein synthesis.
Bacterial cells grown under conditions that favor fast growth and proliferation (i.e., “rich” media) have more ribosomes than those propagated in “poor” media . These observations suggest that the rate of protein synthesis in bacteria is controlled mostly by ribosome numbers . Although growth rate does not seem to affect significantly the fraction of active ribosomes in the cell (≈80%) or their activity , recent observations suggest that even in rich media bacterial ribosomes do not function at maximal elongation rates . Hence, translation rates may be adjusted to proliferation rates by means other than ribosome content.
In budding yeast, although protein synthesis rates decrease with decreasing growth rates, there is no proportional decrease in the number of ribosomes per cell . For example, a 10-fold drop in growth rate is only accompanied by a 2-fold drop in the number of ribosomes per cell (see Table 4 in ). On the other hand, synthesis of ribosomal components is inhibited as cells begin to exhaust the available nutrients and prepare to enter stationary phase , or upon amino acid starvation . Apparently, both the activity and the number of ribosomes may be affected in yeast as a function of growth rate.
In cycling, unperturbed yeast cells, synthesis of ribosomal components is not cell cycle dependent . Interfering with ribosome biogenesis, however, affects cell cycle progression dramatically. In yeast, 59 of a total of 78 ribosomal proteins of cytoplasmic ribosomes are encoded by pairs of very similar or identical paralogous genes . Mutants carrying single deletions of those ribosomal protein genes are usually viable . Many of these deletion strains have a small overall cell size . A small overall cell size is also characteristic of cells lacking Sfp1p, a transcriptional activator of ribosome biosynthesis and ribosomal protein genes . Cells lacking Sfp1p are born very small , and their growth rate is about half of that of wild type cells . As a result, the duration of the G1 phase of the cell cycle is greatly increased in sfp1Δ cells . Still, the smaller critical size threshold of sfp1Δ cells and the smaller overall size of ribosomal protein mutants led Tyers and colleagues to propose that ribosome biogenesis inhibits START in wild type cells . In this model, ribosome biogenesis sets the critical size threshold for START, while translation rates of functional ribosomes enable the cells to pass that threshold . This model appears paradoxical and counterintuitive, especially since in animals ribosome biosynthesis is thought to promote cell proliferation and cancer . But another finding, that ribosomal proteins may function as haploinsufficient tumor suppressors in animals, appeared to offer support for a negative role of ribosome biogenesis in cell division . However, it was subsequently reported that such effects may be due to cell non-autonomous routes . Furthermore, the following observations argue against the notion that ribosome biogenesis has a general inhibitory role for the initiation of division: First, inhibition of ribosome maturation delays START . Second, despite their small cell size, most ribosomal protein mutants have a longer G1 phase . Third, loss-of-function of the vast majority of essential ribosome biogenesis factors leads to G1 arrest (see Table 1 and ). The most straightforward interpretation of the evidence outlined above is that ribosome biogenesis promotes initiation of cell division in budding yeast.
Even when there is a G1 delay due to loss of a ribosomal protein, G1 variables such as birth and critical size of cells lacking individual ribosomal proteins are not uniform, differing qualitatively and quantitatively . Furthermore, although a delay in G1 is the most common phenotype upon loss of a ribosomal protein, this phenotype is not universal. In several cases, there is no cell cycle phenotype, or a G2/M block is observed instead . The basis of all those differences in ribosomal protein mutant phenotypes related to the cell cycle is not clear. Do they reflect specialized translational roles of some ribosomes? Are overall translation rates affected? Is the concentration of ribosomes, their composition, their activity, localization in the cell (or any combination of the above) that is affected? Examples of specialized ribosomal functions abound , leading some to speculate on the existence of a “ribosome code” . There are even cases of extraribosomal roles for ribosomal proteins . Regardless of the answers to the above questions, it is imperative that the relevant mRNA substrates affected in each ribosomal protein mutant must be identified, to understand how cell cycle progression might be impacted. However, as is the case for wild type cells (see INITIATE TO START? above), there are no systematic surveys of mRNAs that are translated differentially in the cell cycle in ribosomal protein mutants.
THE OTHER RIBOSOME SUBSTRATES: tRNAS
For the ribosome to elongate at its maximal rate, all its substrates must be present at saturating concentrations. This includes the aminoacyl-tRNAs and the various elongation factors . Inhibition of elongation factor eEF2 may be one way that protein synthesis is inhibited in animal cells in mitosis . However, unlike the numerous examples of perturbations in translation initiation factors that lead to G1 arrest in yeast (Table 1), there is very little analogous evidence for translation elongation factors affecting cell cycle progression. The only reported example is from a large survey of essential genes, reporting that blocking expression of eEF1Bγ in yeast leads to cell cycle arrest in mitosis (, see Table 1).
Translation elongation rates may be affected by several parameters , including the supply and demand for each tRNA. The genetic code is essentially universal. One and the same codon does not code for different amino acids in different organisms. The code, however, is also degenerate. Most amino acids can be specified by more than one codon. A decades-old speculation has been that codons for an amino acid that are used more frequently in an organism would be translated more rapidly than codons for the same amino acid that are rarely used . Differences in codon usage were difficult to test until the advent of ribosome profiling. Sequencing ribosome-protected mRNA fragments allows estimates of ribosome residency on individual codons . Several analyses that included the original ribosome profiling datasets in yeast  have examined various parameters, including codon usage, and reached contradictory conclusions . Nonetheless, common codons may be translated faster than rare ones in yeast . Modulating which codon is used and the effective concentration of its corresponding tRNA may be a way to influence translation elongation rates both within an mRNA, and across the transcriptome . Surveying codon usage across each codon and tRNA availability revealed that in highly expressed mRNAs rare codons are more prevalent in the first 30-50 codons, slowing down and crowding ribosomes along that stretch . It was proposed that this slow “ramp” is a mechanism that promotes faster translation downstream, by alleviating ribosome “traffic jams” along the mRNA . Furthermore, it turns out that once a particular codon has been used, it will also be used more frequently whenever the same amino acid is encoded downstream in that mRNA . Based on these observations, it was theorized that tRNAs do not diffuse away from the ribosome once they are expelled from it. Instead, the same tRNA for a codon specifying the repeating amino acid is re-charged and channeled for re-use, enabling translation to proceed faster than tRNA diffusion .
The examples outlined above illustrate how alterations in the supply and demand for each tRNA could impact translation rates. The pertinent question for this review, however, is whether such mechanisms could lead to translational control during the cell cycle. Remarkably, a recent study proposed exactly that kind of regulation, based on codon usage . Optimal codon usage is more prevalent in mRNAs expressed in the G1 phase of the cell cycle, implying that the corresponding mRNAs are translated more efficiently . Interestingly, it has been known for decades that loss-of-function mutations in several tRNA synthetases, and even in a tRNA gene, lead to G1 arrest in yeast (see Table 1). Optimizing translation elongation rates in G1 through codon usage is an exciting possibility. But a correlation is not causation, and the above predictions must await experimental validation, measuring the translational efficiencies of the putative mRNA targets in cycling cells. On a cautionary note, a recent study in mouse embryonic stem cells reported that translation elongation rates were not only independent of codon usage, but also very similar across different mRNAs . Likewise, another study in yeast reported that the rate of translation elongation and translational efficiency were not affected by tRNA abundance, and codon translation rates were not correlated with codon bias . Hence, these issues remain controversial and there might be some time before the dust settles.
DIVIDE TO TRANSLATE?
Implicit in the discussion of all the examples mentioned above is the notion that cell growth and protein synthesis drive cell cycle progression, not the other way around. This is generally the case, established in classic and particularly lucid experiments by Hartwell and colleagues . However, there are also some changes in the pattern of growth once cell cycle progression is blocked . Does that mean that progressing in the cell cycle might also affect the translational control of specific mRNAs? The answer is a resounding yes. Ruggero and colleagues examined by ribosome profiling human cells arrested by thymidine block (G1 and S phases) and nocodazole treatment (G2 phase) in the cell cycle, reporting extensive translational control of numerous mRNAs . Interestingly, this work revealed functional clusters of co-regulated mRNAs. Translational control may be used to coordinate expression of specific cellular machines and processes . These experiments are very important, answering how cell division controls translation. However, they do not answer how translation controls cell division.
The role of protein synthesis and translational control has a long history in the cell cycle field. The pioneering experiments of decades ago were incisive, but also largely descriptive. Since then, progress has been incremental and focused on a limited number of putative mRNA translational targets. Identifying all the mRNAs that are under periodic translational control in cycling cells is an obvious and necessary goal. Given the transformative methodologies now available and the current pace of progress, it is only a matter of time before we know how protein synthesis drives cell cycle progression.
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- T. Tuller, I. Veksler-Lublinsky, N. Gazit, M. Kupiec, E. Ruppin, and M. Ziv-Ukelson, "Composite effects of gene determinants on the translation speed and density of ribosomes", Genome Biology, vol. 12, pp. R110, 2011. http://dx.doi.org/10.1186/gb-2011-12-11-r110
- J.B. Plotkin, and G. Kudla, "Synonymous but not the same: the causes and consequences of codon bias", Nature Reviews Genetics, vol. 12, pp. 32-42, 2010. http://dx.doi.org/10.1038/nrg2899
- M. Siwiak, and P. Zielenkiewicz, "A Comprehensive, Quantitative, and Genome-Wide Model of Translation", PLoS Computational Biology, vol. 6, pp. e1000865, 2010. http://dx.doi.org/10.1371/journal.pcbi.1000865
- T. Tuller, Y.Y. Waldman, M. Kupiec, and E. Ruppin, "Translation efficiency is determined by both codon bias and folding energy", Proceedings of the National Academy of Sciences, vol. 107, pp. 3645-3650, 2010. http://dx.doi.org/10.1073/pnas.0909910107
- W. Qian, J. Yang, N.M. Pearson, C. Maclean, and J. Zhang, "Balanced Codon Usage Optimizes Eukaryotic Translational Efficiency", PLoS Genetics, vol. 8, pp. e1002603, 2012. http://dx.doi.org/10.1371/journal.pgen.1002603
- C.A. Charneski, and L.D. Hurst, "Positively Charged Residues Are the Major Determinants of Ribosomal Velocity", PLoS Biology, vol. 11, pp. e1001508, 2013. http://dx.doi.org/10.1371/journal.pbio.1001508
- E.W.J. Wallace, E.M. Airoldi, and D.A. Drummond, "Estimating Selection on Synonymous Codon Usage from Noisy Experimental Data", Molecular Biology and Evolution, vol. 30, pp. 1438-1453, 2013. http://dx.doi.org/10.1093/molbev/mst051
- J. Yang, X. Chen, and J. Zhang, "Codon-by-Codon Modulation of Translational Speed and Accuracy Via mRNA Folding", PLoS Biology, vol. 12, pp. e1001910, 2014. http://dx.doi.org/10.1371/journal.pbio.1001910
- J. Gardin, R. Yeasmin, A. Yurovsky, Y. Cai, S. Skiena, and B. Futcher, "Measurement of average decoding rates of the 61 sense codons in vivo", eLife, vol. 3, 2014. http://dx.doi.org/10.7554/elife.03735
- K. Fredrick, and M. Ibba, "How the Sequence of a Gene Can Tune Its Translation", Cell, vol. 141, pp. 227-229, 2010. http://dx.doi.org/10.1016/j.cell.2010.03.033
- T. Tuller, A. Carmi, K. Vestsigian, S. Navon, Y. Dorfan, J. Zaborske, T. Pan, O. Dahan, I. Furman, and Y. Pilpel, "An Evolutionarily Conserved Mechanism for Controlling the Efficiency of Protein Translation", Cell, vol. 141, pp. 344-354, 2010. http://dx.doi.org/10.1016/j.cell.2010.03.031
- G. Cannarozzi, N.N. Schraudolph, M. Faty, P. von Rohr, M.T. Friberg, A.C. Roth, P. Gonnet, G. Gonnet, and Y. Barral, "A Role for Codon Order in Translation Dynamics", Cell, vol. 141, pp. 355-367, 2010. http://dx.doi.org/10.1016/j.cell.2010.02.036
- M. Frenkel-Morgenstern, T. Danon, T. Christian, T. Igarashi, L. Cohen, Y. Hou, and L.J. Jensen, "Genes adopt non-optimal codon usage to generate cell cycle-dependent oscillations in protein levels", Molecular Systems Biology, vol. 8, 2012. http://dx.doi.org/10.1038/msb.2012.3
- N. Ingolia, L. Lareau, and J. Weissman, "Ribosome Profiling of Mouse Embryonic Stem Cells Reveals the Complexity and Dynamics of Mammalian Proteomes", Cell, vol. 147, pp. 789-802, 2011. http://dx.doi.org/10.1016/j.cell.2011.10.002
- C. Pop, S. Rouskin, N.T. Ingolia, L. Han, E.M. Phizicky, J.S. Weissman, and D. Koller, "Causal signals between codon bias, mRNA structure, and the efficiency of translation and elongation", Molecular Systems Biology, vol. 10, pp. 770-770, 2014. http://dx.doi.org/10.15252/msb.20145524
- A.I. Goranov, and A. Amon, "Growth and division—not a one-way road", Current Opinion in Cell Biology, vol. 22, pp. 795-800, 2010. http://dx.doi.org/10.1016/j.ceb.2010.06.004
- A.I. Goranov, M. Cook, M. Ricicova, G. Ben-Ari, C. Gonzalez, C. Hansen, M. Tyers, and A. Amon, "The rate of cell growth is governed by cell cycle stage", Genes & Development, vol. 23, pp. 1408-1422, 2009. http://dx.doi.org/10.1101/gad.1777309
Work in the authors’ laboratories has been supported with grants from the National Science Foundation (MCB-0818248 to M.P.) and the National Institutes of Health (GM58770 to R.A.). The open access publishing fees for this article have been covered by the Texas A&M University Online Access to Knowledge (OAK) Fund, supported by the University Libraries and the Office of the Vice President for Research.
Translate to divide: сontrol of the cell cycle by protein synthesis by Michael Polymenis and Rodolfo Aramayo is licensed under a Creative Commons Attribution 4.0 International License.


Iconic host of BBC Radio 1’s Essential Mix
and a few other shows as well, Pete Tong has been a staple of the electronic world and has become one of the most recognized UK DJs in the world. Aside from his hosting, Tong also performs around the world at festivals and clubs with a style that features electro, house and deep house.
His sets transition between high energy, repetitive house, and more relaxed vibes. They show off the skill he possesses as a DJ and are masterfully crafted to get the audience into the music. Not one to rush things, Pete prefers to take listeners on a journey through sound instead of going for drop after drop. Below you can find a sample of what you can expect from the legend when he steps up to the decks.
After seeing him last year at Seattle's own Foundation Nighclub
, I highly recommend catching Pete Tong live come this September 28th at Decibel Festival
. Pete Tong will be closing down Decibel as part of his All Gone Pete Tong
set with Tensnake
. This really is something you will not want to miss if you are attending Decibel Festival. He is a master of his craft and one of the all-time greats when it comes to UK DJs and DJs in general. Don’t miss the legend when he returns to Seattle.
For more information on Decibel Festival or Pete Tong, check out the links below.


text:
Good morning everyone!
I hope that everyone is having a wonderful week!
I have two Father’s Day cards to share with you today. Now, normally I would have shared these before Father’s Day, but I didn’t want the recipients to see them before hand.
While the first one is specifically Father’s Day, it would be so simple to switch up the sentiment in the background to something else. Maybe Birthday?
This was such a simple card to make, that I just love! I stamped Father’s Day repeatedly over the background, doing my best to keep things lined up. To (try) to do that, I first stamped the middle line, then did the one above, then the one below. That helped keeps things semi lined up 🙂 That stamp is from the May Paper Pumpkin. I just love the exclusive stamp sets available! The main colors used are the new Dapper Denim, Smokey Slate, and Daffodil Delight.
This was the card for my husband. While we don’t have any children together, we do have 3 fur babies. He spoils them like you wouldn’t believe! So this card was from not only me, but also them lol
I saw a tutorial by Kristina Werner a bit ago. She is an amazing artist on YouTube, but she does a lot of fantastic tutorials. This one was from her “Galaxy” tutorial.
The heart was done on a piece of watercolor paper. I painted it in many colors (it was a MESS!) then went over it with a wash of black watercolor, allowing some of the brighter colors to peek through.Some white ink was splattered onto the paper when the watercolors were dry, to give the appearance of stars.
I then die cut out the heart, adhered it to a piece of Shimmery White cardstock. That was adhered to a piece of retired DSP, then stamped with another retired stamp. Everything here is Stampin’ Up, with exception of the watercolors used.
I took a closeup with the flash, so you can better see the colors showing through.
If you have any questions, let me know! Have a wonderful Wednesday!

domain: hobby


text:
Eczema on scalp
The main challenge with treatment options for scalp eczema is hair. There are numerous remedies for eczema on the scalp but who wants to leave the house with their head plastered in an oily or creamy substance, definitely not a good look!
Treatment for scalp eczema
There is really no choice here as flaky scalp skin equals dandruff and not just a few snowflakes either, think more avalanche. As if this isn’t horrible enough, itching can drive you crazy plus drive away your work colleagues who will fear the worst. I mean, who really wants head lice! Treatment for eczema on your scalp is something you will certainly need to positively embrace.
What does eczema on the scalp look like?
Symptoms involve irritated and inflamed red areas, dry skin which flakes off and oozes and possibly infected lesions. The scalp will feel angry, sore and crusty.
The symptoms mimic other disorders like Psoriasis and Rosacea so a proper diagnosis is essential.
Pictures of eczema on the scalp
Sometimes pictorial identification from images is simpler to match up rather than a wordy description which parallels loads of diseases. Peruse our pictures of eczema on the scalp ranging in severity from mild to severe examples.
What causes scalp eczema?
Scientists and doctors know what it is – a persistent, chronic inflammation, the technical name for which is Seborrheic Dermatitis.
The sebaceous glands located in the scalp race into overdrive and produce too much sebum, a combo of oil and wax. What triggers them to do this still remains a mystery.
Learn how to treat eczema on your scalp
Treatment for scalp eczema priorities removing the itch, reducing redness and weakening and loosening the scale. Depending on how bad the eczema is, some people find that using a proprietary shampoo several times a week is sufficient. Popular types include coal tar not without controversy and which belongs to a drug category rather alarmingly called keratoplastics. Other alternatives are selenium sulphide and zinc pyrithione. Normal usage is to alternate with your own so in reality, how to treat eczema on your scalp is neither too onerous nor very time-consuming.
Don’t pull your hair out!
There are treatments available for eczema of the scalp but why not consider a change of hairstyle or even a wig for those all important calendar dates…job interviews, parties, weddings. Clever styling from a talented hairdresser or trichologist, the latter a certified specialist in hair and disorders of the scalp, can disguise an unattractive scaly head, gone are the days of just trying to wear a hat, whatever the occasion. A low soft bun style covers the skin behind the ears and at the nape of the neck.
Curls and waves provide density and coverage over the top of the scalp through shaping and bounce. Loose slightly ruffled braids conceal eczema at the front of the scalp on the forehead, avoid the cornrow tight plaits of some designs. Men, who don’t tend to favour long locks, can struggle more with concealment but slightly baggy or shaggy looks work well. An appropriate expert can also advise on camouflage through colouring and the use of non-chemical based dyes. They can be a real complement to your own home remedies and normal routine.
How to treat really bad scalp eczema
If washing alone doesn’t tackle it then your clinician may prescribe mild corticosteroids which will be topical not oral. These are for use in acute flare-ups. There are non-steroid based substitutes such as Elidel for mild cases which is a TCI, Topical Calcineurin Inhibitor manufactured to adjust the immune response. Tacrolimus ointment is for middling to serious cases.
Are there home remedies for eczema on the scalp?
Some people just don’t want to resort to chemical or drug-based intervention, preferring to learn how to remove this pernicious condition more naturally, holistically and hopefully, in an enduring manner. There are lots of herbal and gentle therapies which you may even already have lurking in your bathroom cabinet or kitchen cupboard.
Apple cider vinegar is a fragrant cooling rinse after you have washed your hair, always dilute first. Coconut oil mixed with a plain shampoo yields great results at cooling sensitivity, peppermint oil likewise. Minty essential oil makes for a great massage treatment diluted with a base or carrier oil, for instance, olive oil or lavender.
Some home remedies for eczema on the scalp are so fruitful and potent at elimination that you will be celebrating in your new found knowledge of how to cure scalp eczema.
And with such lovely scented and fragrant choices, you will hardly feel you are losing out, forced to resort to the skin disorder aisle in the drug store.
Babies with eczema
This is known colloquially as ‘cradle cap’ and is often easier to access on a baby or very young child as many newborns simply have less hair. Experienced mums know how to treat this and it is not uncommon. If it persists then speak to your midwife or health worker as this may require a different solution. Never use anything on baby’s scalp that is not approved for infant use.
How to Remove Scars – Best Remedies and Removal Procedures That Actually Work.
Anyone who has been alive long enough will have scars. Whether from surgeries, acne, chickenpox, or injuries the scars start out as pinkish makes which
What soap is best for Eczema on body: liquid and natural solutions
They tutor us as children to believe that washing our hands automatically cleans away all germs. doctors also use soap to scrub up before a
Discoid Eczema: diagnosis, symptoms, causes, treatment, pictures
Discoid eczema is also frequently called nummular eczema or discoid dermatitis. The rash occurs between the ages of 55 to 65 and is more prevalent
How to Get rid of Eczema on Legs: Symptoms, Treatments, remedies.
Eczema is commonly found on the legs as well as a number of other extremities. The sensitive skin and nature of location make it a
Atopic Dermatitis Eczema treatment: Natural home remedies with pictures
There are many kinds of eczema, but atopic dermatitis eczema is the most prevalent. They believe the causes to be both genetic and external. After
What is Eczema Herpeticum: Symptoms, diagnosis and treatment
Imbalance in our bodies will always migrate up to the surface. This is the case with eczema herpeticum which is a result of the herpes

domain: medical


text:
VENUE AND TRAVEL INFO
TRAVEL REQUIREMENTS FOR TOURISTS TO SINGAPORE
Singapore strongly encourages visitors to check for eligibility and specific requirements based on the country they will be travelling from. Learn more about the details on travelling responsibly to and around Singapore by clicking the link below.
MARINA BAY SANDS
Click the link below for complete address details, maps, parking, directions, and other details on how to get to Marina Bay Sands.
Don’t forget everything you need to bring before going to Singapore. Get more information from the link below.

domain: geography


Ecology & conservation jobs
Broaden your search
Refine your search
Found 2 Temp jobs
We’re looking for a Chief Operating Officer who can make an invaluable addition to our executive team.
Surfers Against Sewage (SAS) is one of the UK's leading marine conservation and campaigning charities. Our mission is simple: to Create Ocean Activ...
Neath Port Talbot Council are looking for a Countryside and Wildlife Team Leader to join our team.
You will also work alongside the UKCEH Enterprise Board to build on the existing research contracts with the private sector & licensed information.


text:
i love ceviche, all sorts of ceviche and i get more excited to make ceviche when i see fresh sea food which happens very often in san francisco.:-) i try my own variations and add other ingredients to give it a different flavor every time.
this time i used some fresh sea bass as the main ingredient and gave it a persian flavor with some saffron and lime juice.
- two sea bass fillets
- half of a white onion
- chopped fresh cilantro
- chopped fresh dille
- one teaspoon of saffron
- two fresh limes
- one cup of chopped mango
- one cup of chopped pineapple
- fresh ground sea salt and pepper
cut the fish fillets in small slices. chop the onion in tiny pieces and add to the fish. chop the herbs and fruits and add them to the mix. press the limes into it and add olive oil, salt, and pepper. dissolve the saffron in a small cup of hot water and add to the mix. leave them in the fridge and let it cool for four to six hours. serve it martini glasses or if you don't have any like me use some wide red wine glasses. enjoy it with crackers or your favorite chips. i used some magnificent carrot and purple potato chips from wholefoods. nousheh jahn!

domain: food


text:
The surname Lymburner was first found in Essex where they held a family seat as Lords of the Manor. The Saxon influence of English history diminished after the Battle of Hastings in 1066. The language of the courts was French for the next three centuries and the Norman ambience prevailed. But Saxon surnames survived and the family name was first referenced in the 13th century when they held lands.
This web page shows only a small excerpt of our Lymburner research. Another 70 words (5 lines of text) covering the years 1455 and 1487 are included under the topic Early Lymburner History in all our PDF Extended History products and printed products wherever possible.
Some of the first settlers of this family name were:
Lymburner Settlers in Canada in the 18th Century
John Lymburner, who settled in Montreal in 1766
Adam Lymburner, who arrived in Quebec in 1775
Mrs. Margaret Lymburner U.E. (née) Kaims (b. 1747) born in Scotland from Maine, USA who settled in Saint John, New Brunswick c. 1783, then Ontario, Canada she was married to Matthew Lymburner who died 1788 in New Brunswick
Mr. Matthew Lymburner Jr., U.E. who settled in Canada c. 1784
Mr. John Lymburner U.E. who settled in Home District [York County], Ontario c. 1784
Lymburner Settlers in Canada in the 20th Century
Louis Lymburner, aged 49, who settled in Montreal, Canada, in 1920
Marie Lymburner, aged 47, who immigrated to Montreal, Canada, in 1920
J.H. Lymburner, American assistant pilot to Lincoln Ellsworth on his expedition, eponym of Mount Lymburner, Antarctica
Mr. Adam Lymburner MacNider (1778-1840), born in Quebec, prominent merchant and auctioneer in Montreal, Director of the Montreal Savings Bank 1819, in 1820 he was commissioned an ensign, by 1828 he became captain serving through till 1838, 1821 he helped to establish the General Hospital, he served as Grand Juror 1824 – 1827, Justice of the peace in 1830, commissioner on the Montreal Board of Health in 1832 during the Cholera epidemic
Peter Lymburner Robertson (1879-1951), Canadian inventor of the square-drive Robertson screw
^ Rubincam, Milton. The Old United Empire Loyalists List. Genealogical Publishing Co., Inc, 1976. (Originally published as; United Empire Loyalists. The Centennial of the Settlement of Upper Canada. Rose Publishing Company, 1885.) ISBN 0-8063-0331-X
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domain: history


text:
Gubernatorial Hopeful Coakley Attending Pittsfield Festival
Massachusetts attorney general and Democratic candidate for governor Martha Coakley will be in Pittsfield tomorrow for the city’s street festival.Less than three weeks before state primaries on Sept. 9, Coakley, a North Adams native, will visit downtown Pittsfield for 3rd Thursday. Showcasing the area’s food, culture and arts the street festival is held monthly from May to October.
“I know that the creative economy across the commonwealth is very exciting both for the opportunities it gives for our individuals in Massachusetts [and] it’s also a good economic driver,” said Coakley.
Coakley is being challenged by fellow Democrat and state Treasurer Steve Grossman along with Don Berwick. Republican Charlie Baker, Tea Party candidate Mark Fisher and Independents Jeff McCormick, Evan Falchuk and Scott Lively are also running. The festival starts at 5 p.m. Thursday on North St.

domain: politics


text:
US Sanctions Iranian Judge Complicit in Christian Persecution
Sanctions Send a Message of Hope to Iran’s Christian Community
12/19/2019 Washington D.C. (International Christian Concern) – International Christian Concern (ICC) has learned that on December 19, 2019, the United States issued financial sanctions against two Iranian judges complicit in violating the human rights of Iranians. One of these judges, Mohammad Moghisseh, has a long record of specifically violating the rights of Iran’s Christian minority.
“Through their respective branches of Revolutionary Courts, Abolghassem Salavati and Mohammad Moghisseh, both designated today, oversaw the Iranian regime’s miscarriage of justice in show trials in which journalists, attorneys, political activists, and members of Iran’s ethnic and religious minority groups were penalized for exercising their freedom of expression and assembly and sentenced to lengthy prison terms, lashes, and even execution,” said the United States Treasury Department in a statement.
Earlier this year, ICC recommended the name of Judge Mohammad Moghisseh for sanctions, specifically because of his ongoing abuse of Iranian Christians. His record of persecution includes specific patterns of engaging in double jeopardy sentencing and being complicit in the medical abuse of imprisoned Christians. Many of Iran’s incarcerated Christians were sent to prisons which Judge Moghisseh had once helped manage. He rose through the judicial ranks because of his hardline stance in support of the regime’s human rights abuses.
Matias Perttula, ICC’s Advocacy Director, said, “The steps taken by the United States government today are definitely the right way forward, and we celebrate the work of the Department of the Treasury’s Office of Foreign Assets Control to move forward with sanctions. This decision will bring hope to the people of Iran and especially to those who have suffered under the cruelty of the Iranian regime’s so-called ‘judicial system.’ While the steps taken by the US government are welcomed, more can be done to advance human rights and religious freedom for all Iranians. The US must continue to rally with its allies and maintain consistent pressure on the Iranian regime to bring change. ICC was honored to give voice in this process.”
All property and interests of those designated by today’s sanctions are thereby blocked. Any financial institution that facilitates these judges’ transactions risks exposure to these sanctions and having its own access to the US financial system severed.
Claire Evans, ICC’s Regional Manager for the Middle East, said, “The sanctioning of an Iranian Revolutionary Court judge is a powerful message to send to Iran. It shows that individuals complicit in horrific human rights abuses will be held accountable, and cannot hide behind governmental institutions. For Christians who are always subjected to abuses perpetrated by Iran’s Revolutionary Courts, this sends a strong message of hope. A reminder that they are not forgotten, and that we stand with them in their struggle for freedom of conscience.”

domain: news


text:
This post is also available in: Français
How to Find Us
Although in a conservation area, we are not far from civilisation; in fact we are just minutes away from the AP7 (junction 751 Los Montesinos) and on the main road km13 on the CV95 Torrevieja/Orihuela Road.
We are close to the towns of San Miguel de Salinas and Torremendo and the historical town of Orihuela. Just 15 minutes away are the coastal towns of Guardamar and Torrevieja with their excellent beaches. We are also within easy travelling distance of some of the Costa Blanca’s popular golf areas such as Algorfa, Villamartin.
Access to airports is extremely good, with an approximate 40 minute drive from Alicante airport and a 30 minute drive to Murcia’s San Javier airport.
If you use a sat nav simply enter the following co-ordinates into your unit.
38.0211623,-0.845900, or 38°01’16.2″N 0°50’45.2″W
From Alicante – Motorway, AP7
Take the Junction 751, follow directions on the roundabout to Orihuela/ Bigastro, on the CV945, until you come to the CV95, turn right and see directions below. *CV95
From Murcia – Motorway AP7
You can either stay on the Motorway and get off at Junction 751 as above and follow the directions to the CV95 or avoid the toll road and get off at Campoamor. Follow the signs to San Miguel, and once you are through San Miguel follow the directions to Orihuela/Bigastro on the CV95. *see below CV95. Note the CV95 goes in both directions, you MUST NOT GO to Torrevieja. Access to Orihuela Bigastro is straight out of San Miguel, direction Los Montesinos and just under bridge you will see turning on your right for Orihuela CV95.
Travel straight through Los Montesinos on the CV945 over the motorway until you reach the CV95 or get onto the CV95 off the N332, drive past the Torrevieja Hospital, past San Miguel de Salinas.
On the CV95 you will pass the 13km marker and almost immediately look out for the turning into the CV950 on your right, marked Torreaguera. See *CV950 for further details.
The CV95 Is the road the links Torrevieja to Orihuela and runs past the Torrevieja Hospital. We are mid-way (between the 12km & 13km mark) along this stretch of road. It can be accessed from many directions.
*CV95 – You need to travel along the CV95 for a while, DO NOT TAKE THE TORREMENDO TURNOFF (OR ANY OTHER TURNOFF), Continue until you pass Restaurants Vista Bella & La Fortaleza (between the 13km & 12km mark). On the crest of the hill you will find a turning into the CV950 marked Torreaguera/Embalse la Pedrera.
* The CV950 encircles the lake.
Directions from Vistabella:
Driving north on the CV95, just past the 13km indicator you will see the Fortaleza Restaurant on your right and Vistabella Restaurant on left. Then on your left you can see our office – Costa Blanca Quad Tours.
– Continue past our office on the CV95.
– At the top of the hill turn left into the CV950 marked Embalse de la Pedrera / Torreagiera.
– Drive 700m along the CV950 (less than a km) See wind turbine.
– Turn left at sign La Pedrera, (yellow sign with 2 horses)
– Drive up the hill and around corner.
– Drive down just past the third black gate on the corner – La Pedrera, Gate 2 – Go through the NO ENTRY signs and park up on the left.
– Take the short walk back to Gate 2 as pictured and press intercom on the left at Gate 2 for attention and check-in.


text:
Yield: 4 Servings
|1 cup||Chicken stock|
|10||Tomatillos (husked); rinsed and chopped|
|1 cup||Onions; chopped|
|2||Serrano chiles; seeded and chopped|
|2 tablespoons||Fresh cilantro; chopped|
|Salt; to taste|
|¼ cup||Chicken stock|
|2 cups||Black beans; cooked|
|1||Clove garlic; minced|
|2||Serrano chiles; seeded and minced|
|½ cup||Mango or papaya; diced|
|4||Scallions (white part only); thinly sliced|
|½ cup||Corn kernels; roasted|
|8 ounces||Fresh goat cheese; crumbled|
|Salt; to taste|
|Vegetable oil; to soften tortillas|
|1 cup||Mango Relish (separate recipe)|
Preheat the oven to 350 degrees F.
To make the sauce, in a saucepan, cook the chicken stock, tomatillos, garlic cloves, onions, and serranos over medium-high heat for 10 minutes, stirring frequently. Transfer the mixture to a blender, add the cilantro, and puree until smooth. Season with salt and set aside.
To make the filling, in another saucepan, bring all the filling ingredients except the cheese and salt to a boil. Remove from the heat, whisk in 4 ounces of the goat cheese, and season with salt. Deep warm.
Pour enough of the oil in a skillet to come ½ inch up the sides. Over medium heat, bring the oil to 350 degrees F. or just smoking. (CAUTION: Do This Very Carefully--This is VERY, VERY HOT--) Submerge the tortillas in the oil one by one for 5 seconds each to soften. Drain the tortillas on paper towels and keep warm: do not stack the tortillas.
To assemble the enchiladas, divide the black bean-goat cheese mixture evenly among the tortillas, spreading evenly down the middle. Roll up the tortillas and place seam side down on a baking sheet or in an ovenproof baking dish, placing them snugly together. Pour the reserved tomatillo sauce over the enchiladas, and top with the remaining 4 ounces of the goat cheese. Cover with foil and bake in the oven for 10 minutes. Serve 2 enchiladas per plate, together with Mango Relish (separate recipe).
Chef's Notes: This recipe is included by chef Stephan Pyles in his cookbook __The New Texas Cuisine__, Doubleday, 1993, ($35.00).
The chef states: "This recipe was published in _Parade_ magazine in 1987 in an article commissioned by my friend Sheila Lukins... Although at first glance this combination may not seem very Texan, one only has to realize that the Gulf Coast is subtropical and that some of the best goat cheese in the country is made here in Dallas by the Mozzarella Company." (He's right!)
Posted to MC-Recipe Digest V1 #214 Date: 23 Aug 96 17:17:10 EDT
From: Paul & Terri Law <103366.1520@...> NOTES : "Black beans, goat cheese, and mango have become a popular combination
in the new Texas cooking, and once you've tasted these enchiladas, you'll understand the appeal" says Chef Pyles of Star Canyon in Dallas, Texas.


text:
Satellite image of Cyclone Bola near peak intensity
|Formed||February 24, 1988|
|Dissipated||March 4, 1988|
|Highest winds||10-minute sustained:
165 km/h (105 mph)
195 km/h (120 mph)
|Lowest pressure||940 mbar (hPa); 27.76 inHg|
|Damage||$82 million (1988 USD)|
|Areas affected||Fiji, Vanuatu, New Zealand|
|Part of the 1987–88 South Pacific cyclone season|
Cyclone Bola was one of the costliest cyclones in the history of New Zealand, causing severe damage as an extratropical cyclone when it passed near the country in March 1988. It formed on February 24 to the north of Fiji, and tracking generally southwestward it reached hurricane-force winds near Vanuatu on February 28. The next day it generated peak wind velocities of 195 km/h (120 mph), though it quickly weakened as it accelerated southward. On March 4 Bola transitioned into an extratropical storm, passing to the north of the North Island of New Zealand on March 8. It weakened further and was absorbed by a stationary trough near the South Island on March 12.
The cyclone first affected Fiji, where it produced gale force winds and strong waves. In Vanuatu, Bola dropped heavy rainfall, which destroyed two bridges and caused severe damage to islands in the group. Bola caused severe damage to the North Island of New Zealand, where heavy rainfall peaked at 917 mm (36.1 in) in Gisborne Region. Damage totaled over $82 million (1988 USD). Three people were killed due to flooding, and hundreds were evacuated when a swollen river threatened Wairoa. The name Bola was later retired, meaning it will not be used again within the same basin.
On February 24, 1988, the Fiji Meteorological Service's Nadi Tropical Cyclone Warning Center (TCWC Nadi) started to monitor a tropical depression that had developed within the South Pacific Convergence Zone to the north-northeast of Suva, Fiji. During that day the system moved towards the southwest, before the Joint Typhoon Warning Center (JTWC) initiated warnings on the system and designated it as Tropical Cyclone 13P after it had become equivalent to a tropical storm. Over the next 2 days the system gradually developed tropical cyclone characteristics as it moved south-westwards and passed to the northwest of Fiji. TCWC Nadi subsequently named the system Bola during February 26, after it had become equivalent to a modern day category 1 tropical cyclone on the Australian tropical cyclone intensity scale.
Bola gradually intensified as its movement slowed and stalled, and on February 28 the Joint Typhoon Warning Center (JTWC) assessed the cyclone as reaching hurricane-force winds near Vanuatu. It turned to a southeast drift before executing a small cyclonic loop on March 1, during which the JTWC estimated Bola attained peak winds of 195 km/h (120 mph). At the same time, its minimum central pressure was estimated at 940 mbar.
After reaching peak intensity, Cyclone Bola quickly weakened as it accelerated southeastward toward a frontal trough. On March 3, its winds dropped below hurricane-force, and it gradually lost its tropical characteristics. The structure became asymmetric, with a large band of clouds extending well south of the circulation. By March 4, Bola had completed the transition into an extratropical cyclone. Which turned south and began to affect the North Island of New Zealand on March 6. A building ridge of high pressure to its south caused the extratropical remnants of Bola to slow and turn to the west on March 7. The next day, the storm passed about 110 km (70 mi) north of the North Island. Around the same time, the storm began slowly filling, meaning the low pressure area associated with Bola was losing its identity. It turned southward on March 9, and on March 12 was absorbed by a stationary trough in the Westerlies near the western coast of the South Island.
Fiji and Vanuatu
As a tropical cyclone, Bola first impacted Fiji shortly after forming while passing to the northwest, and again as it was weakening after peak intensity to the southwest of the island. It brushed the country with gale force winds and waves of up to 5 m (16.4 ft). Severe damage was reported throughout the archipelago, however the Fijian Government did not assess how much damage was done.
Cyclone Bola remained near Vanuatu for about a week, during which it reached its peak intensity while executing a cyclonic loop. The most affected locations were Epi island, the Shepherd Islands, and the islands in Malampa Province, and throughout the country the cyclone affected more than 15,000 people and 3,000 houses. In a five-day period the cyclone dropped about 450 mm (17.7 in) of rainfall. Two bridges on Malakula were destroyed, and several other bridges were flooded or damaged. The passage of the cyclone also left several buildings, roads, and crop fields damaged.
Cyclone Bola created some of the heaviest rainfall totals for a single storm in the history of New Zealand, with some locations receiving more than half of their annual rainfall totals from the storm. While the cyclone passed north of the island, a strong easterly flow over the North Island contained the interaction between moist air from Bola and drier air from the ridge to its southeast. In the Gisborne region, the flow resulted in the heaviest rainfall totals, when the moisture ascended over the region's western mountainous areas and condensed into precipitation. One station recorded 419 mm (16.5 in) in a 24 hour period. The maximum rainfall total attributed to the storm was 917 mm (36.1 in), reported at a station near Tolaga Bay. Heavy rainfall totals of up to and over 300 mm (12 in) were observed in the regions of Auckland and Northland. The cyclone is the largest to be recorded in 93 years of rainfall records. As such, it had a large and lasting effect on the rivers of the area when it deposited a large amount of sediment, as recorded in the sedimentary record of Lake Tutira. Shortly prior to losing its identity, the remnants of Bola also dropped 100–200 mm (4–8 in) of precipitation on the South Island of New Zealand.
Storm damage was heaviest in Gisborne, where rain destroyed or damaged several roads and bridges. Three days of continuous rainfall led to mudslides, flooding, and erosion. Flooding killed three people when a car was swept away. In Te Karaka in Gisborne, a flooded river forced 500 residents to evacuate. A total of 1,765 farmers were affected by the flooding, accounting for about 3,600 hectares (8,900 acres) of damaged crop fields and about $90 million in crop damage (1988 NZD, $82 million 1988 USD. Water supplies were disrupted in two cities due to flooding. Rainfall in Northland Region caused flooding and outages to telephone and power. Additionally, beginning on about 6 March, the cyclone began affecting the North Island with strong easterly winds of over hurricane force, caused by the interaction between the extratropical remnants of Bola and a ridge of high pressure to its south. The winds damaged a few homes, including some in which the roofs were damaged or destroyed. In addition, the strong winds downed several trees, and at the same time, erosion and landslides left hillsides bare without grass or trees.
In Vanuatu, cyclone victims received food and emergency aid following the storm. Australian patrol boat HMAS Cessnock provided manpower assistance to 11 islands in the country. Reconstruction costs in Vanuatu totalled about $5 million (1988 USD), which was about 10 percent of the country's national budget.
After the passage of the storm, four towns in New Zealand declared states of emergency. The New Zealand government provided about $80 million (1988 NZD) to the east coast region of the North Island for assisting in cyclone damage. $8 million was used to create an East Coast Forestry Conservation Scheme, which was set to protect forests and prevent erosion. A study was taken five years after the storm, consisting of a group of 112 people who were evacuated or received monetary assistance in response to the cyclone; the study showed 12% of the respondents as experiencing Posttraumatic stress disorder, of which they reported a general lack of assistance and public support.
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- World Meteorological Organization
- Fiji Meteorological Service
- Meteorological Service of New Zealand
- Joint Typhoon Warning Center