Language

English

Publication Date

2-1-2023

Journal

The FASEB Journal

DOI

10.1096/fj.202201481R

PMID

36607631

PMCID

PMC10129296

PubMedCentral® Posted Date

4-25-2023

PubMedCentral® Full Text Version

Author MSS

Abstract

SOHLH1 and NOBOX are oocyte-expressed transcription factors with critical roles in ovary development and fertility. In mice, Sohlh1 and Nobox are essential for fertility through their regulation of the oocyte transcriptional network and cross-talk to somatic cells. Sumoylation is a posttranslational modification that regulates transcription factor function, and we previously showed that mouse oocytes deficient for sumoylation had an altered transcriptional landscape that included significant changes in NOBOX target genes. Here, we show that mouse SOHLH1 is modified by SUMO2/3 at lysine 345 and mutation of this residue alters SOHLH1 nuclear to cytoplasmic localization. In NOBOX, we identify a non-consensus SUMO site, K97, that eliminates NOBOX mono-SUMO2/3 conjugation, while a point mutation at K125 had no effect on NOBOX sumoylation. However, NOBOX

Keywords

Animals, Female, Mice, Basic Helix-Loop-Helix Transcription Factors, Homeodomain Proteins, Lysine, Oocytes, Ovary, Sumoylation, Transcription Factors

Published Open-Access

yes

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