rotein unique to the testis HSF5 is necessary for transcriptional reprogramming and appropriate chromatin architecture, which propel the development of pachynema.

• R Kummari

  English

  Author

• C Bhagvati

  English

  Author

During mammalian meiotic prophase I,
chromatin remodeling and transcriptional
reprogramming are crucial processes, but the
exact mechanisms governing these processes are
still unclear. Our earlier research showed that
male infertility and meiotic arrest are caused by
the loss of heat shock factor 5 (HSF5), a member
of the heat shock factor family. Nevertheless, the
molecular mechanisms by which HSF5 controls
meiotic development remain unclear. The
function of HSF5 in regulating chromatin
dynamics and transcriptional reprogramming
during pachynema progression was examined in
this work using a thorough multi-omics
approach. Significant changes in chromatin
accessibility and disruption of the transcriptional
regulatory network (TRN) were found in
Hsf5−/− spermatocytes, according to analysis of
ATAC-seq and single-cell RNA sequencing
data. Furthermore, poor XY body formation and
abnormal histone modifications were caused by
HSF5 loss. Significantly, Hsf5−/−
spermatocytes also showed aberrant
spermatoproteasome activity on sex
chromosomes. There is evidence that HSF5 may
in vivo form a complex with USP7 to reduce
H2AK119ub on meiotic sex chromosomes.
These results enhance our knowledge of HSF5's
function during pachynema progression and
shed fresh light on its intricate, multifaceted
involvement in controlling important meiotic
processes.

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