Heterochromatin and Toxic YChromosomes

许多生物的Y染色体含有大量的转座子，它们是 转录上受到抑制的染色质标记的限制。当解除了这些表观遗传 经过修饰，许多TES可以很容易地从一个基因组位置移动到另一个基因组位置(有毒Y 染色体)。然而，在进化过程中，年轻的Y染色体仍然包含大量必需的 被活跃转录的基因，以及相互对立的机制之间的竞争 异染色质的形成和活跃的转录可导致TES不完全沉默 进化中的Y染色体。 我们的建议旨在描述宿主特定基因和自私基因之间的表观遗传冲突 在退化的不同阶段，进化中的Y染色体上的元素，其分辨率可能选择 用于Y。 Y染色体上重复元素的积累在性行为中似乎是普遍存在的 染色体进化。我们将利用果蝇进化的neo-Y染色体 不同程度的退化，使用表达谱和 染色质分析。我们将在neo-Y染色体上连接表观遗传学和表达谱， 在基因和重复密度上的差异，以鉴定基因在neo-Y上的活跃转录 染色体导致TES的不完全沉默。我们将确定有毒的Y染色体 通过形成突变负担和降低男性寿命，导致男性健康成本，如 根据我们的初步工作建议。将我们的结果整合到AIMS中，将提供有关 Y染色体的毒性如何随时间变化，以及宿主之间的表观遗传冲突是如何发生的 基因和自私因素可能会被解决。

Y chromosomes of many organisms contain a large number of transposable elements (TEs), which are transcriptionally constrained by repressive chromatin marks. When relieved of these epigenetic modifications, many TEs can readily move from one genomic location to another (toxic Y chromosomes). Yet evolutionarily young Y chromosomes still contain a large number of essential genes that are actively transcribed, and competition between the opposing mechanisms of heterochromatin formation and active transcription can result in incomplete silencing of TEs on evolving Y chromosomes. Our proposal aims to characterize epigenetic conflicts between host-specific genes and selfish genetic elements on evolving Y chromosomes at various stages of degeneration, whose resolution may select for adaptive degeneration of the Y. The accumulation of repetitive elements on the Y chromosome appears to be universal during sex chromosome evolution. We will take advantage of evolving neo-Y chromosomes in Drosophila with varying levels of degeneration, to catalog toxicity of Y chromosomes using expression profiling and chromatin analysis. We will link epigenetic and expression profiles across neo-Y chromosomes that differ in gene and repeat density, to identify whether active transcription of genes on neo-Y chromosomes results in incomplete silencing of TEs. We will establish whether toxic Y chromosomes incur a fitness cost on males, by forming a mutational burden and reducing male longevity, as suggested by our preliminary work. Integrating our results across aims will provide a full picture of how the toxicity of the Y chromosome changes over time, and how epigenetic conflicts between host genes and selfish elements may be resolved.