Heterochromatin and Toxic YChromosomes

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.

Grant Number: 5R01GM101255-11
NIH Institute/Center: NIH
Principal Investigator: Doris Bachtrog