scholarly journals MRG‐1 is required for both chromatin‐based transcriptional silencing and genomic integrity of primordial germ cells in Caenorhabditis elegans

2019 ◽  
Vol 24 (5) ◽  
pp. 377-389 ◽  
Author(s):  
Takashi Miwa ◽  
Kunio Inoue ◽  
Hiroshi Sakamoto
Keyword(s):  
Caenorhabditis Elegans ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Transcriptional Silencing ◽  
Genomic Integrity

scholarly journals MRG-1 is required for genomic integrity in Caenorhabditis elegans germ cells

Cell Research ◽  
2012 ◽  
Vol 22 (5) ◽  
pp. 886-902 ◽  
Author(s):  
Jing Xu ◽  
Xiaojuan Sun ◽  
Yudong Jing ◽  
Mo Wang ◽  
Kai Liu ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Germ Cells ◽  
Genomic Integrity

MES-2, a maternal protein essential for viability of the germline in Caenorhabditis elegans, is homologous to a Drosophila Polycomb group protein

Development ◽  
1998 ◽  
Vol 125 (13) ◽  
pp. 2457-2467 ◽  
Author(s):  
R. Holdeman ◽  
S. Nehrt ◽  
S. Strome
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Germ Cells ◽  
Target Genes ◽  
Essential Feature ◽  
Primordial Germ Cells ◽  
Polycomb Group ◽  
Polycomb Group Protein ◽  
Maternal Contribution ◽  
Group Protein

A unique and essential feature of germ cells is their immortality. In Caenorhabditis elegans, germline immortality requires the maternal contribution from four genes, mes-2, mes-3, mes-4 and mes-6. We report here that mes-2 encodes a protein similar to the Drosophila Polycomb group protein, Enhancer of zeste, and in the accompanying paper that mes-6 encodes another Polycomb group protein. The Polycomb group is responsible for maintaining proper patterns of expression of the homeotic and other genes in Drosophila. It is thought that Polycomb group proteins form heteromeric complexes and control gene expression by altering chromatin conformation of target genes. As predicted from its similarity to a Polycomb group protein, MES-2 localizes to nuclei. MES-2 is found in germline nuclei in larval and adult worms and in all nuclei in early embryos. By the end of embryogenesis, MES-2 is detected primarily in the two primordial germ cells. The correct distribution of MES-2 requires the wild-type functions of mes-3 and mes-6. We hypothesize that mes-2 encodes a maternal regulator of gene expression in the early germline; its function is essential for normal early development and viability of germ cells.

scholarly journals PRMT5 Protects Genomic Integrity during Global DNA Demethylation in Primordial Germ Cells and Preimplantation Embryos

2014 ◽  
Vol 56 (4) ◽  
pp. 564-579 ◽  
Author(s):  
Shinseog Kim ◽  
Ufuk Günesdogan ◽  
Jan J. Zylicz ◽  
Jamie A. Hackett ◽  
Delphine Cougot ◽  
...  
Keyword(s):  
Germ Cells ◽  
Primordial Germ Cells ◽  
Dna Demethylation ◽  
Preimplantation Embryos ◽  
Genomic Integrity

scholarly journals The Role of Mutant p63 in Female Fertility

2021 ◽  
Vol 22 (16) ◽  
pp. 8968
Author(s):  
Yi Luan ◽  
Pauline Xu ◽  
Seok-Yeong Yu ◽  
So-Youn Kim
Keyword(s):  
Germ Cells ◽  
Essential Role ◽  
Primordial Germ Cells ◽  
Genomic Integrity ◽  
Biological Functions ◽  
Ovarian Insufficiency ◽  
P53 Family ◽  
C Terminus ◽  
N Terminus

The transcription factor p63, one of the p53 family members, plays an essential role in regulating maternal reproduction and genomic integrity as well as epidermal development. TP63 (human)/Trp63 (mouse) produces multiple isoforms: TAp63 and ΔNp63, which possess a different N-terminus depending on two different promoters, and p63a, p63b, p63g, p63δ, and p63ε as products of alternative splicing at the C-terminus. TAp63 expression turns on in the nuclei of primordial germ cells in females and is maintained mainly in the oocyte nuclei of immature follicles. It has been established that TAp63 is the genomic guardian in oocytes of the female ovaries and plays a central role in determining the oocyte fate upon oocyte damage. Lately, there is increasing evidence that TP63 mutations are connected with female infertility, including isolated premature ovarian insufficiency (POI) and syndromic POI. Here, we review the biological functions of p63 in females and discuss the consequences of p63 mutations, which result in infertility in human patients.

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