The Oocyte-Specific Linker Histone H1FOO Is Not Essential for Mouse Oogenesis and Fertility
Fernando Sánchez-Sáez,
Raquel Sainz-Urruela,
Natalia Felipe-Medina,
Yazmine B. Condezo,
Manuel Sánchez-Martín,
Elena Llano,
Alberto M. Pendás
Affiliations
Fernando Sánchez-Sáez
Molecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca, 37007 Salamanca, Spain
Raquel Sainz-Urruela
Molecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca, 37007 Salamanca, Spain
Natalia Felipe-Medina
Molecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca, 37007 Salamanca, Spain
Yazmine B. Condezo
Molecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca, 37007 Salamanca, Spain
Manuel Sánchez-Martín
Departamento de Medicina, Universidad de Salamanca, 37007 Salamanca, Spain
Elena Llano
Molecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca, 37007 Salamanca, Spain
Alberto M. Pendás
Molecular Mechanisms Program, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca, 37007 Salamanca, Spain
Meiosis is a highly conserved specialized cell division process that generates haploid gametes. Many of its events are associated with dynamically regulated chromosomal structures and chromatin remodeling, which are mainly modulated by histone modifications. Histone H1 is a linker histone essential for packing the nucleosome into higher-order structures, and H1FOO (H1 histone family, member O, oocyte-specific) is a H1 variant whose expression pattern is restricted to growing oocytes and zygotes. To further explore the function of H1FOO, we generated mice lacking the H1foo gene by the CRISPR/Cas9 technique. Herein, we combine mouse genetics and cellular studies to show that H1foo-null mutants have no overt phenotype, with both males and females being fertile and presenting no gross defects in meiosis progression nor in synapsis dynamics. Accordingly, the histological sections show a normal development of gametes in both male and female mice. Considering the important role of oocyte constituents in enhancing mammalian somatic cell reprogramming, we analyzed iPSCs generation in H1foo mutant MEFs and observed no differences in the absence of H1FOO. Taken all together, in this work we present the first in vivo evidence of H1FOO dispensability for mouse fertility, clarifying the debate in the field surrounding its essentiality in meiosis.
