Abstract
Intragenomic conflict describes a phenomenon in which genetic elements act ‘selfishly’ to gain a transmission advantage at the expense of the whole genome. A non-essential, selfish B chromosome known as Paternal Sex Ratio (PSR) induces complete elimination of the sperm-derived hereditary material in the jewel wasp Nasonia vitripennis. PSR prevents the paternal chromatin from forming chromosomes during the first embryonic mitosis, leading to its loss. Although paternally transmitted, PSR evades self-elimination in order to be inherited. We examined important post-translational modifications to the DNA packaging histones on the normal genome and the PSR chromosome in the fertilized embryo. Three histone marks – H3K9me2,3, H3K27me1, and H4K20me1 – became abnormally enriched and spread to ectopic positions on the sperm’s chromatin before entry into mitosis. In contrast, other histone marks and DNA methylation were not affected by PSR, suggesting that its effect on the paternal genome is specific to a subset of histone marks. Contrary to the paternally derived genome, the PSR chromosome was visibly devoid of the H3K27me1 and H4K20me1 marks. These findings strongly suggest that PSR causes paternal genome elimination by disrupting at least three histone marks following fertilization, while PSR avoids self-elimination by evading two of these marks.
Highlights
Intragenomic conflict describes a phenomenon in which genetic elements act ‘selfishly’ to gain a transmission advantage at the expense of the whole genome
One of the most striking examples of intragenomic conflict stems from a non-essential, supernumerary B chromosome known as Paternal Sex Ratio (PSR), which is present in natural populations of the jewel wasp Nasonia vitripennis[5,6]
In order to better understand the nature of paternal genome elimination by PSR, we used fluorescent-based tools to microscopically visualize the dynamics of several key post-translational histone modifications in young wild type and PSR-carrying embryos
Summary
Intragenomic conflict describes a phenomenon in which genetic elements act ‘selfishly’ to gain a transmission advantage at the expense of the whole genome. PSR-induced elimination of the sperm-derived genome compliment converts female-destined embryos into males that carry and transmit PSR. This effect leads to severely male-biased wasp populations, an effect that inspired the naming of PSR when it was originally detected[5,9]. The paternal chromatin fails to lose its phosphorylation of histone H3 at Serine residue 10 (H3S10p) at the end of this first division[7] This mark is believed to be necessary for proper condensation and resolution of chromatin into chromosomes at the onset of nuclear division through the activity of Condensin[10,11,12]. What remains to be determined, is whether PSR directly causes these chromatin defects in order to block chromosome resolution of the paternal set or, instead, acts indirectly through disruption of other upstream chromatin-based processes
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