More mog genes that influence the switch from spermatogenesis to oogenesis in the hermaphrodite germ line of Caenorhabditis elegans

Abstract

The Caenorhabditis elegans XX animal possesses a hermaphrodite germ line, producing first sperm, then oocytes. In this paper, we report the genetic identification of five genes, mog-2, mog-3, mog-4, mog-5, and mog-6, that influence the hermaphrodite switch from spermatogenesis to oogenesis. In mog-2-mog-6 mutants, spermatogenesis continues past the time at which hermaphrodites normally switch into oogenesis and no oocytes are observed. Therefore, in these mutants, germ cells are transformed from a female fate (oocyte) to a male fate (sperm). The fem-3 gene is one of five genes that acts at the end of the germline sex determination pathway to direct spermatogenesis. Analyses of mog;fem-3 double mutants suggest that the mog-2-mog-6 genes act before fem-3; thus these genes may be in a position to negatively regulate fem-3 or one of the other terminal regulators of germline sex determination. Double mutants of fem-3 and any one of the mog mutations make oocytes. Using these double mutants, we show that oocytes from any mog;fem-3 double mutant are defective in their ability to support embryogenesis. This maternal effect lethality indicates that each of the mog genes is required for embryogenesis. The two defects in mog-2-mog-6 mutants are similar to those of mog-1: all six mog genes eliminate the sperm/oocyte switch in hermaphrodites and cause maternal effect lethality. We propose that the mog-2-mog-6 mutations identify genes that act with mog-1 to effect the sperm/oocyte switch. We further speculate that the mog-1-mog-6 mutations all interfere with translational controls of fem-3 and other maternal mRNAs.

The Caenorhabditis elegans Sex Determination Gene mog-1 Encodes a Member of the DEAH-Box Protein Family

“…To identify trans-acting factors that repress fem-3 via its 3Ј UTR, both genetic and molecular approaches have been taken. A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six mog (for masculinization of the germ line) genes (18,19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for fem-3 binding factor), a homolog of Drosophila Pumilio that binds specifically to the fem-3 PME regulatory element (46). FBF is encoded by one of two nearly identical genes, fbf-1 and fbf-2, and therefore is not likely to have been identified in the genetic screens for mog mutants.…”

“…Among the various mog genes, mog-1 is best characterized genetically (18). Four mog-1 alleles were isolated, and null mutants were identified by genetic tests.…”

“…Four mog-1 alleles were isolated, and null mutants were identified by genetic tests. The mog-1 gene is required zygotically for the sperm-oocyte switch, a rather specific developmental function, and maternally for embryogenesis (18). Using double-mutant analysis, mog-1 was placed upstream of fem-3 and, therefore, in a reasonable genetic position to function as a fem-3 repressor.…”

“…Using double-mutant analysis, mog-1 was placed upstream of fem-3 and, therefore, in a reasonable genetic position to function as a fem-3 repressor. However, the genetic position of mog-1 also lies upstream of fem-1, fem-2, fog-1, and fog-3, four other genes required for the specification of germ cells as sperm (12,18). Therefore, mog-1 might regulate any of these genes to effect the sperm-oocyte switch.…”

Competence for Chemical Reprogramming of Sexual Fate Correlates with an Intersexual Molecular Signature inCaenorhabditis elegans

“…To ask whether competence for U0126 gamete sex reprogramming is a common feature of XX sperm-only adults, we tested a battery of mutants, all with a fully penetrant phenotype of germline masculinization: puf-8 fbf-1 (Bachorik and Kimble 2005), fem-3(gf) (Barton et al 1987), mog-1 (Graham and Kimble 1993), fbf-1; lip-1 (this work), and puf-8 fbf-1; lip-1 (this work). As a positive control, we also assayed puf-8; lip-1, which was previously identified as competent for chemical reprogramming (Morgan et al 2010).…”