1,037 research outputs found
Panel Discussion On Lipid Metabolism In Cardiovascular Disease†
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111126/1/jgs00741.pd
Anderson Localization, Non-linearity and Stable Genetic Diversity
In many models of genotypic evolution, the vector of genotype populations
satisfies a system of linear ordinary differential equations. This system of
equations models a competition between differential replication rates (fitness)
and mutation. Mutation operates as a generalized diffusion process on genotype
space. In the large time asymptotics, the replication term tends to produce a
single dominant quasispecies, unless the mutation rate is too high, in which
case the populations of different genotypes becomes de-localized. We introduce
a more macroscopic picture of genotypic evolution wherein a random replication
term in the linear model displays features analogous to Anderson localization.
When coupled with non-linearities that limit the population of any given
genotype, we obtain a model whose large time asymptotics display stable
genotypic diversityComment: 25 pages, 8 Figure
Slit1 and Slit2 Cooperate to Prevent Premature Midline Crossing of Retinal Axons in the Mouse Visual System
AbstractDuring development, retinal ganglion cell (RGC) axons either cross or avoid the midline at the optic chiasm. In Drosophila, the Slit protein regulates midline axon crossing through repulsion. To determine the role of Slit proteins in RGC axon guidance, we disrupted Slit1 and Slit2, two of three known mouse Slit genes. Mice defective in either gene alone exhibited few RGC axon guidance defects, but in double mutant mice a large additional chiasm developed anterior to the true chiasm, many retinal axons projected into the contralateral optic nerve, and some extended ectopically—dorsal and lateral to the chiasm. Our results indicate that Slit proteins repel retinal axons in vivo and cooperate to establish a corridor through which the axons are channeled, thereby helping define the site in the ventral diencephalon where the optic chiasm forms
Quaking RNA bindings proteins as mediator of oncolytic HSV vectors in huma hepatoma cells
Comunicaciones a congreso
Impact of sequencing depth in ChIP-seq experiments
In a chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) experiment, an important consideration in experimental design is the minimum number of sequenced reads required to obtain statistically significant results. We present an extensive evaluation of the impact of sequencing depth on identification of enriched regions for key histone modifications (H3K4me3, H3K36me3, H3K27me3 and H3K9me2/me3) using deep-sequenced datasets in human and fly. We propose to define sufficient sequencing depth as the number of reads at which detected enrichment regions increase <1% for an additional million reads. Although the required depth depends on the nature of the mark and the state of the cell in each experiment, we observe that sufficient depth is often reached at <20 million reads for fly. For human, there are no clear saturation points for the examined datasets, but our analysis suggests 40–50 million reads as a practical minimum for most marks. We also devise a mathematical model to estimate the sufficient depth and total genomic coverage of a mark. Lastly, we find that the five algorithms tested do not agree well for broad enrichment profiles, especially at lower depths. Our findings suggest that sufficient sequencing depth and an appropriate peak-calling algorithm are essential for ensuring robustness of conclusions derived from ChIP-seq data
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