Replication Timing of Amplified Genetic Regions Relates to Intranuclear Localization but Not to Genetic Activity or G/R Band

Amplified genes in many human cancer cells usually localize at the extrachromosomal double minutes (DMs). In the present study, we show that multiple DMs in the human colorectal tumor COLO 320DM line replicated semisynchronously during the early S phase. On the other hand, during longer passage of the cells with DMs, cells with the amplified genes at the chromosomal homogeneously staining region (HSR) generally dominate the population. We currently report that HSR was composed of a tandem array of DM-derived sequences, which was shown using a unique DM-painting probe. Nevertheless, we found that HSR was replicated much later during the S phase, unless the amplified c-myc genes were expressed almost equally from DMs and HSR. Therefore, this provided a novel instance in which the cytogenetic localization affected replication timing without alteration of expression. Furthermore, we unexpectedly found that HSR had a distinctive band structure with respect to replication timing. The replication band structure was usually associated with the chromosomal G/R bands; however, HSR was homogeneous in the G/R band and in the distribution of highly repetitive sequences. We discuss the mechanism by which the replication band may arise, in relation to the folding of chromatin inside the nucleus.     

Timing of propagule release significantly alters the deposition area of resulting aerial dispersal

Aim The aim of this study is to determine whether changes to the seasonal and circadian timing of propagule release can a have a significant effect on the area covered by resulting aerial dispersal. Location Western Australia. Methods Using the atmospheric pollution model (TAPM), an existing meso‐scale dispersal model, a range of release patterns was simulated and the resulting deposition compared. Comparisons were based on observations of deposition patterns and the calculated area of deposition. Results Small changes to the timing of propagule release were shown to significantly impact on the area experiencing deposition from the resulting aerial dispersal. Main conclusions Simulations performed in this study show that, for small propagules, changes to the timing of release can lead to alternate, clearly differentiable dispersal events. Small changes in both the seasonal and circadian patterns of release can have significant effects on the area that experiences deposition during the resulting dispersal event. This effect is particularly important at the landscape scale and when there is a need to quantify individual dispersal events. Predictive modelling of aerial dispersal needs to be undertaken with an understanding of the manner in which biological and environmental factors that affect the timing of propagule release can influence results. Results presented highlight the need to characterize the epidemiology of pathogenic organisms of importance to biosecurity as much as possible before they arrive.     

Why is timing of bird migration advancing when individuals are not?

Recent advances in spring arrival dates have been reported in many migratory species but the mechanism driving these advances is unknown. As population declines are most widely reported in species that are not advancing migration, there is an urgent need to identify the mechanisms facilitating and constraining these advances. Individual plasticity in timing of migration in response to changing climatic conditions is commonly proposed to drive these advances but plasticity in individual migratory timings is rarely observed. For a shorebird population that has significantly advanced migration in recent decades, we show that individual arrival dates are highly consistent between years, but that the arrival dates of new recruits to the population are significantly earlier now than in previous years. Several mechanisms could drive advances in recruit arrival, none of which require individual plasticity or rapid evolution of migration timings. In particular, advances in nest-laying dates could result in advanced recruit arrival, if benefits of early hatching facilitate early subsequent spring migration. This mechanism could also explain why arrival dates of short-distance migrants, which generally return to breeding sites earlier and have greater scope for advance laying, are advancing more rapidly than long-distance migrants.     

Genomic Basis of Circannual Rhythm in the European Corn Borer Moth

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Cell line differences in replication timing of human glutamate receptor genes and other large genes associated with neural disease

There is considerable current interest in the function of epigenetic mechanisms in neuroplasticity with regard to learning and memory formation and to a range of neural diseases. Previously, we described replication timing on human chromosome 21q in the THP-1 human cell line (2n = 46, XY) and showed that several genes associated with neural diseases, such as the neuronal glutamate receptor subunit GluR-5 (GRIK1) and amyloid precursor protein (APP), were located in regions where replication timing transitioned from early to late S phase. Here, we compared replication timing of all known human glutamate receptor genes (26 genes in total) and APP in 6 different human cell lines including human neuron-related cell lines. Replication timings were obtained by integrating our previously reported data with new data generated here and information from the online database ReplicationDomain. We found that many of the glutamate receptor genes were clearly located in replication timing transition zones in neural precursor cells, but this relationship was less clear in embryonic stem cells before neural differentiation; in the latter, the genes were often located in later replication timing zones that displayed DNA hypermethylation. Analysis of selected large glutamate receptor genes (>200 kb), and of APP, showed that their precise replication timing patterns differed among the cell lines. We propose that the transition zones of DNA replication timing are altered by epigenetic mechanisms, and that these changes may affect the neuroplasticity that is important to memory and learning, and may also have a role in the development of neural diseases.     

Evening chronotype,late weekend sleep times and social jetlag as possible causes of sleep curtailment after maintaining perennial DST: ain’t they as black as they are painted?

ABSTRACT

People sleep less in response to setting social clocks earlier relative to the sun clocks. We proposed here a model-based approach for estimating sleep loss as the difference between weekend and weekday risetimes divided on the difference between weekend risetime and weekday bedtime. We compared this approach with a traditional approach to estimating sleep curtailment as the difference in weekly average sleep duration in two conditions. Weekday and weekend sleep times reported for 320 samples provided possibility of testing whether evening types with later weekend sleep times and larger social jetlag differ from morning types with earlier weekend sleep times and smaller social jetlag on amount of sleep lost (1) throughout the week and (2) in response to an advance of weekday wakeups, for instance, after the expected installation of perennial Daylight Saving Time (DST). We found that (1) an amount of sleep lost due to advancing shift of weekday wakeups depends upon neither chronotype nor weekend sleep times nor social jetlag, (2) a very large amount of sleep is usually lost by evening types with later weekend sleep times and larger social jetlag and (3) an essential sleep loss is caused by our usual work/school schedules, even in morning types with early weekend sleep times and small social jetlag. As compared to such permanent sleep losses experienced by any types, an additional loss due to switching from Standard Time (ST) to perennial DST are expected to be relatively small. We also found that the traditional way of calculation of sleep curtailment leads to paradoxical conclusions, such as (1) sleep loss is larger when social jetlag is smaller, not larger, (2) sleep loss is larger when weekend sleep times are earlier, not later, (3) despite 1-h difference between two student samples in weekday wakeups, their sleep losses can be identical.     

Seasonal variation in the response of Hagberg falling and liquefaciton numbers to propiconazole fungicide in wheat

The hypothesis was tested that seasonal differences in the response to propiconazole fungicide of hagberg failling and liquefaction numbers are related to grain drying rate, as indicated by potential evaportranspiration. The response of Hagberg failling and liquefaciton numbers to late-season applicaitions of propiconazole was calculated using data from a field experiments in each of the years 1981 to 1990 on winter wheat (Triticum aestivum) cv. Agalong grown with similar husbandry at one site. Cumulative potential evapotranspiration was calculated over seven different periods during grain ripening. No visible sprouting occurred in any experiment and Hagberg falling number was above 250 s in nine of the 10 years. Disease severity on the flag leaf was less than 7% in nine of the 10 years, and diseases were generally controlled well by propiconazole. There were no significant relationships between the response of Hagberg falling number and any of the potential evapotranspiration variables. The response of liquefaction number was exponentially related to each of three cumulative potential evapotranspiration variables which covered periods before the estimated date of 40% moisture content. Years with lower cumulative potential evapotranspiration gave the greater responses, but the relationships were considerably influenced by the two lowest potential evapotranspiration years. It was concluded that these data provide indirect evidence that the response of Hagberg falling number (when transformed to liquefaction number) to fungicide is mediated through grain drying rate, and furthermore that the results are compatible with the hypothesis that pre-maturity alpha-amylase activity is stimulated by slow grain drying.