Transmission of an entire human chromosome through the mouse male germline reveals an unexpectedly high tolerance of aneuploidy during male meiosis and results in accurate transcriptional deployment despite massive epigenetic remodeling during spermatogenesis.
Chromosome segregation in male spermatocytes exhibits anaphase A without shortening of autosome-associated microtubules and partitioning of an unpaired X chromosome that is initiated by an imbalance of attached kinetochore microtubules.
Biochemical and genetic approaches uncover a chromatin remodeler for PRDM9 binding and the parallel local epigenetic modification of cytosines in mouse spermatocytes.
The meiotic recombination landscape in vertebrates was re-engineered via the co-evolution of a dual histone H3K4/H3K36 methylation 'writer' PRDM9 and its 'reader' ZCWPW1 that facilitates efficient double strand break repair.
Post-transcriptional control by YTHDC2 is required to turn off the mitotic proliferation program and facilitate proper expression of the meiotic program to allow a clean cell fate transition in the germline stem cell lineage.
Prdm9-generated meiotic asynapsis of homologous chromosomes in mouse subspecific hybrids causes hybrid sterility and can be reversed by introducing random stretches of consubspecific sequence (≥ 27Mb) on four chromosomes most sensitive to asynapsis.
Female-inherited supernumerary chromosomes that lack a male-inherited homolog are transmitted to all meiotic products instead of the expected half, which indicates an additional amplification of unpaired chromosomes during meiosis.
Analysis of a spermiogenesis protein reveals a new chromatin requirement for synchrony between maternal DNA packaged in the egg and sperm-packaged paternal DNA in the first embryonic mitosis in Drosophila melanogaster.
Variation in codon usage among functional categories of human genes is not due to selection for translation efficiency, but to differences in intragenic recombination rate, linked to variation in meiotic transcription level.
