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

1999 ◽  
Vol 19 (3) ◽  
pp. 2189-2197 ◽  
Author(s):  
Alessandro Puoti ◽  
Judith Kimble

ABSTRACT In the Caenorhabditis elegans hermaphrodite germ line, the sex-determining gene fem-3 is repressed posttranscriptionally to arrest spermatogenesis and permit oogenesis. This repression requires a cis-acting regulatory element in the fem-3 3′ untranslated region; the FBF protein, which binds to this element; and at least six mog genes. In this paper, we report the molecular characterization of mog-1 as well as additional phenotypic characterization of this gene. Themog-1 gene encodes a member of the DEAH-box family. Threemog-1 alleles possess premature stop codons and are likely to be null alleles, and one is a missense mutation and is likely to retain residual activity. mog-1 mRNA is expressed in both germ line and somatic tissues and appears to be ubiquitous. The MOG-1 DEAH-box protein is most closely related to proteins essential for splicing in the yeast Saccharomyces cerevisiae, but splicing appears to occur normally in a mog-1-null mutant. In addition to its involvement in the sperm-oocyte switch and control of fem-3, zygotic mog-1 is required for robust germ line proliferation and for normal growth during development. We suggest that mog-1 plays a broader role in RNA regulation than previously considered.

Genetics ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 1061-1072 ◽  
Author(s):  
E E Capowski ◽  
P Martin ◽  
C Garvin ◽  
S Strome

Abstract To identify genes that encode maternal components required for development of the germ line in the nematode Caenorhabditis elegans, we have screened for mutations that confer a maternal-effect sterile or "grandchildless" phenotype: homozygous mutant hermaphrodites produced by heterozygous mothers are themselves fertile, but produce sterile progeny. Our screens have identified six loci, defined by 21 mutations. This paper presents genetic and phenotypic characterization of four of the loci. The majority of mutations, those in mes-2, mes-3 and mes-4, affect postembryonic germ-line development; the progeny of mutant mothers undergo apparently normal embryogenesis but develop into agametic adults with 10-1000-fold reductions in number of germ cells. In contrast, mutations in mes-1 cause defects in cytoplasmic partitioning during embryogenesis, and the resulting larvae lack germ-line progenitor cells. Mutations in all of the mes loci primarily affect the germ line, and none disrupt the structural integrity of germ granules. This is in contrast to grandchildless mutations in Drosophila melanogaster, all of which disrupt germ granules and affect abdominal as well as germ-line development.


Genetics ◽  
1997 ◽  
Vol 145 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Lisa C Kadyk ◽  
Eric J Lambie ◽  
Judith Kimble

The germ line is the only tissue in Caenorhabditis elegans in which a stem cell population continues to divide mitotically throughout life; hence the cell cycles of the germ line and the soma are regulated differently. Here we report the genetic and phenotypic characterization of the glp-3 gene. In animals homozygous for each of five recessive loss-of-function alleles, germ cells in both hermaphrodites and males fail to progress through mitosis and meiosis, but somatic cells appear to divide normally. Germ cells in animals grown at 15° appear by DAPI staining to be uniformly arrested at the G2/M transition with <20 germ cells per gonad on average, suggesting a checkpoint-mediated arrest. In contrast, germ cells in mutant animals grown at 25° frequently proliferate slowly during adulthood, eventually forming small germ lines with several hundred germ cells. Nevertheless, cells in these small germ lines never undergo meiosis. Double mutant analysis with mutations in other genes affecting germ cell proliferation supports the idea that glp-3 may encode a gene product that is required for the mitotic and meiotic cell cycles in the C. elegans germ line.


1980 ◽  
Vol 74 (2) ◽  
pp. 446-469 ◽  
Author(s):  
William B. Wood ◽  
Ralph Hecht ◽  
Stephen Carr ◽  
Rebecca Vanderslice ◽  
Nurit Wolf ◽  
...  

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1351-1364 ◽  
Author(s):  
S Hekimi ◽  
P Boutis ◽  
B Lakowski

Abstract We carried out a genetic screen for viable maternal-effect mutants to identify genes with a critical function relatively early in development. This type of mutation would not have been identified readily in previous screens for viable mutants and therefore could define previously unidentified genes. We screened 30,000 genomes and identified 41 mutations falling into 24 complementation groups. We genetically mapped these 24 loci; only two of them appear to correspond to previously identified genes. We present a partial phenotypic characterization of the mutants and a quantitative analysis of the degree to which they can be maternally or zygotically rescued.


Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 43-61 ◽  
Author(s):  
T Schedl ◽  
J Kimble

Abstract This paper describes the isolation and characterization of 16 mutations in the germ-line sex determination gene fog-2 (fog for feminization of the germ line). In the nematode Caenorhabditis elegans there are normally two sexes, self-fertilizing hermaphrodites (XX) and males (XO). Wild-type XX animals are hermaphrodite in the germ line (spermatogenesis followed by oogenesis), and female in the soma. fog-2 loss-of-function mutations transform XX animals into females while XO animals are unaffected. Thus, wild-type fog-2 is necessary for spermatogenesis in hermaphrodites but not males. The fem genes and fog-1 are each essential for specification of spermatogenesis in both XX and XO animals. fog-2 acts as a positive regulator of the fem genes and fog-1. The tra-2 and tra-3 genes act as negative regulators of the fem genes and fog-1 to allow oogenesis. Two models are discussed for how fog-2 might positively regulate the fem genes and fog-1 to permit spermatogenesis; fog-2 may act as a negative regulator of tra-2 and tra-3, or fog-2 may act positively on the fem genes and fog-1 rendering them insensitive to the negative action of tra-2 and tra-3.


Genetics ◽  
1980 ◽  
Vol 95 (2) ◽  
pp. 317-339
Author(s):  
George N Cox ◽  
John S Laufer ◽  
Meredith Kusch ◽  
Robert S Edgar

ABSTRACT Eighty-eight mutants of C. elegans that display a roller phenotype (a helically twisted body) have been isolated and characterized genetically and phenotypically. The mutations are located in 14 different genes. Most genes contain a number of alleles. Their distribution among the chromosomes appears nonrandom, with seven of the genes being located on linkage group 11, some very closely linked. The phenotypes of the mutants suggest that there are five different classes of genes, each class representing a set of similar phenotypic effects: Left Roller (four genes), Right Roller (one gene), Left Squat (one gene), Right Squat (two genes) and Left Dumpy Roller (six genes). The classes of mutants differ with respect to a number of characteristics that include the developmental stages affected and the types of aberrations observed in cuticle structure. A variety of gene interactions were found, arguing that these genes are involved in a common developmental process. The presence of alterations in cuticle morphology strongly suggests that these genes are active in the formation of the nematode cuticle.


Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 143-150
Author(s):  
Jean-Claude Labbé ◽  
Siegfried Hekimi ◽  
Luis A Rokeach

Abstract The Ro ribonucleoproteins (RoRNP) consist of at least one major protein of 60 kD, Ro60, and one small associated RNA, designated Y RNA. Although RoRNP have been found in all vertebrate species examined so far, their function remains unknown. The Caenorhabditis elegans rop-1 gene previously has been identified as encoding a Ro60 homologue. We report here the phenotypic characterization of a C. elegans strain in which rop-1 has been disrupted. This is the first report regarding the inactivation of a major RoRNP constituent in any organism. The rop-1 mutant worms display no visible defects. However, at the molecular level, the disruption of rop-1 results in a dramatic decrease in the levels of the ROP-1-associated RNA (CeY RNA). Moreover, transgenic expression of wild-type rop-1 partially rescues the levels of CeY RNA. Considering that transgenes are poorly expressed in the germline, the fact that the rescue is only partial is most likely related to the high abundance of the CeY RNA in the adult germline and in embryos. The developmental expression pattern and localization of CeY RNA suggest a role for this molecule during embryogenesis. We conclude that, under laboratory culture conditions, ROP-1 does not play a crucial role in C. elegans.


Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 597-608 ◽  
Author(s):  
Elizabeth De Stasio ◽  
Catherine Lephoto ◽  
Lynn Azuma ◽  
Charles Holst ◽  
Dinesh Stanislaus ◽  
...  

Phenotypic reversion of the rubber-band, muscle-defective phenotype conferred by unc-93(e1500) was used to determine the utility of N-ethyl-N-nitrosourea (ENU) as a mutagen for genetic research in Caenorhabditis elegans. In this system, ENU produces revertants at a frequency of 3 × 10–4, equivalent to that of the commonly used mutagen, EMS. The gene identity of 154 ENU-induced revertants shows that the distribution of alleles between three possible suppressor genes differs from that induced by EMS. A higher percentage of revertants are alleles of unc-93 and many fewer are alleles of sup-9 and sup-10. Three revertants complement the three known suppressor genes; they may therefore identify a new gene product(s) involved in this system of excitation-contraction coupling in C. elegans. Molecular characterization of putative unc-93 null alleles reveals that the base changes induced by ENU are quite different from those induced by EMS; specifically we see an increased frequency of A/T → G/C transitions. The frequency of ENU-induced intragenic deletions is found to be 13%. We suggest that ENU, at concentrations below 5 mm, will be a superior mutagen for studies of protein function in C. elegans.


Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 199-210 ◽  
Author(s):  
T R Clandinin ◽  
P E Mains

Abstract Genetic evidence suggests that the mei-1 locus of Caenorhabditis elegans encodes a maternal product required for female meiosis. However, a dominant gain-of-function allele, mei-1(ct46), can support normal meiosis but causes defects in subsequent mitotic spindles. Previously identified intragenic suppressors of ct46 lack functional mei-1 activity; null alleles suppress only in cis but other alleles arise frequently and suppress both in cis and in trans. Using a different screen for suppressors of the dominant ct46 defect, the present study describes another type of intragenic mutation that also arises at high frequency. These latter alleles appear to have reduced meiotic activity and retain a weakened dominant effect. Characterization of these alleles in trans-heterozygous combinations with previously identified mei-1 alleles has enabled us to define more clearly the role of the mei-1 gene product during normal embryogenesis. We propose that a certain level of mei-1 activity is required for meiosis but must be eliminated prior to mitosis. The dominant mutation causes mei-1 activity to function at mitosis; intragenic trans-suppressors act in an antimorphic manner to inactivate multimeric mei-1 complexes. We propose that inactivation of meiosis-specific functions may be an essential precondition of mitosis; failure to eliminate such functions may allow ectopic meiotic activity during mitosis and cause embryonic lethality.


Genetics ◽  
1995 ◽  
Vol 141 (3) ◽  
pp. 977-988 ◽  
Author(s):  
M Maduro ◽  
D Pilgrim

Abstract A spontaneous mutation affecting locomotion of the nematode Caenorhabditis elegans has been mapped to a new gene, unc-119. Phenotypic characterization of the mutants suggests the defect does not lie in the musculature and that the animals also have defects in feeding behavior and chemosensation. unc-119 has been physically mapped relative to a previously identified chromosomal break in linkage group III, and DNA clones covering the region can rescue the mutant phenotype in transgenic animals. Three more alleles at the locus, with identical phenotypes, have been induced and characterized, all of which are putative null alleles. The predicted UNC-119 protein has no significant similarity to other known proteins. Expression of an unc-119/lacZ fusion in transgenic animals is seen in many neurons, suggesting that the unc-119 mutant phenotype is due to a defect in the nervous system.


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