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Genetic Instability and Chromatin Remodeling in Spermatids
Tiphanie Cavé1, Rebecka Desmarais2, Chloé Lacombe-Burgoyne3
1Department of Biochemistry, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Quebec J1E4K8, Canada. tiphanie.cave@usherbrooke.ca.
Genes
|January 17, 2019
Summary
Spermatid chromatin remodeling involves DNA double-strand breaks (DSBs) that are repaired. This process may explain the male mutation bias and generate genetic variations in offspring.
Area of Science:
- Reproductive Biology
- Genetics
- Molecular Biology
Background:
- Spermatids undergo extensive chromatin remodeling, replacing histones with protamines.
- This process involves complex orchestration of histone variants and modifications.
- Evidence suggests this transition is not genetically inert, with transient DNA breaks observed.
Purpose of the Study:
- To investigate the genetic implications of chromatin remodeling in spermatids.
- To characterize the formation and repair of DNA double-strand breaks (DSBs) during spermiogenesis.
- To explore the potential link between post-meiotic DNA breaks and male mutation bias.
Main Methods:
- Detection of DNA breaks using 3'OH end labeling in spermatids.
- Comparative analysis of post-meiotic DNA fragmentation conservation (human to yeast).
- Genome-wide mapping of DSB distribution in a mouse model.
Main Results:
- A significant number of DSBs are formed and repaired in the haploid spermatid stage.
- The process appears to be a reversible enzymatic activity, distinct from apoptosis.
- Post-meiotic DNA fragmentation is conserved across species, from humans to yeast.
- Tools were developed for mapping DSB distribution in the mouse genome.
Conclusions:
- Post-meiotic DSB formation and repair in spermatids may contribute to male mutation bias.
- Chromatin remodeling in spermatids provides a context for inducing genetic variations.
- These variations, including de novo polymorphism and structural changes, can be heritable.
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