Developmentally regulated expression during gametogenesis of the murine gene meg1 suggests a role in meiosis

Abstract

Previous studies have shown that in adult male mice, expression of the meg1 gene is restricted to meiotic and early postmeiotic testicular germ cells. We have now analyzed the expression of meg1 during postnatal testicular development and the comparable meiotic stages in the female. The 0.75 kb transcript for meg1 begins to accumulate in testes at d8-9 of postnatal (pn) development, coincident with the entry of germ cells into meiosis, and is expressed most abundantly at pn d14 and subsequent stages, when the spermatocytes have entered pachytene. In situ hybridization analysis shows that meg1 is expressed at very low levels in leptotene cells and increases as the cells progress through zygotene and pachytene stages. In the embryonic ovary, meg1 is not detected until after day 15 of gestation when the cells have entered the pachytene stage of meiosis I. In situ hybridization analysis suggests that meg1 transcripts are expressed at higher levels in degenerating rather than in healthy pachytene stage oocytes; meg1 is not expressed in any cells of the adult ovary, regardless of the stage of follicular development. These results suggest that meg1 is indeed a meiosis-associated gene in both male and female germ cells through the pachytene stage of meiosis I and appears to exhibit sex-specific differences in its expression thereafter.

Haploinsufficiency for the murine orthologue of Chlamydomonas PF20 disrupts spermatogenesis

“…Although the exact function of the nuclear 35-kDa PF20 protein in spermatogenesis remains to be elucidated, we have identified at least one interacting partner, MEIG1, a chromosome͞chromatin-binding protein initially expressed at meiosis but retained in the nucleus through later stages of spermatogenesis (21)(22)(23). MEIG1 is thought to play a role in meiosis in female and male germ cells, but its presence in postmeiotic male germ cells in conjunction with the current findings raises the possibility that it participates in regulation of chromosome structure and͞or gene expression after meiosis is completed, a function that is presumably impaired in the absence of 35-kDa PF20.…”

A Novel Testis-Specific Metallothionein-like Protein,Tesmin,Is an Early Marker of Male Germ Cell Differentiation

“…Although a considerable number of such genes have been cloned, 41% of the sequence tags from normal testis were found to represent novel cDNAs (Pawlak et al, 1995). Genes that are specifically expressed during male germ cell differentiation include kinases, such as PGK-2 (Tamaru et al, 1990), ferT Keshet et al, 1990), Mak protein kinase (Matsushime et al, 1990;Jinno et al, 1993), TESK1 (Toshima et al, 1995), TSPY (Schnieders et al, 1996), tsHMG (Alami-Ouahabi et al, 1996), Hox-1.4 (Propst et al, 1988), members of the HSP70 gene family (Sarge et al, 1994), PGAM-M (Broceno et al, 1995), meg-1 (Don and Wolgemuth, 1992;Don et al, 1994), calmegin (Watanabe et al, 1994), testis-specific transcription elongation factor S-II (Ito et al, 1996), and TB-RBP (Gu et al, 1998). Gli family members are preferentially expressed during the initial stages of spermatogenesis involving the mitotic proliferation of early precursor cells (Persengiev et al, 1997).…”

Copy Number Variants in Premature Ovarian Failure and Ovarian Dysgenesis

“…Knockout of Meig1 gene causes male infertility in mice because of delayed kinetics in early meiotic stages and impairment of late spermiogenesis [Zhang et al, 2009;Salzberg et al, 2010]. Although female knockout mice show no effects in fertility, it is known that Meig1 is differentially expressed in the embryonic ovary, suggesting that human MEIG1 may play a role in female reproduction [Don et al, 1994]. SMAD6 (mothers against decapentaplegic, Drosophila, homolog of, 6) belongs to the inhibitory SMADs and is induced in response to BMP (bone morphogenetic protein) signaling.…”