scholarly journals MORE SEX-DETERMINATION MUTANTS OF CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (3) ◽  
pp. 649-664 ◽  
Author(s):  
Jonathan Hodgkin
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Constitutive Expression ◽  
Complementation Group ◽  
Sperm Production ◽  
Recessive Mutations ◽  
Her 2 ◽  
Map Location ◽  
Her Genes

ABSTRACT Sex determination in Caenorhabditis elegans is controlled by the X chromosome: autosome ratio, i.e. 2A;XX animals are hermaphrodite, and 2A;XO animals are male. A procedure for isolating 2A;XO animals that are transformed into hermaphrodites has been developed. Nine mutations causing this transformation have been obtained: eight are recessive, and all of these fall into a new autosomal complementation group, her-1 V. The remaining mutation (her-2) is dominant and has a genetic map location similar to that of tra-1 III. Recessive mutations of tra-1 cause the reverse transformation, transforming 2A;XX animals into males. Therefore, the her-2 mutation may result in constitutive expression of tra-1. Mutations in her-1 are without effect on XX animals, but the her-2 mutation prevents sperm production in both XX and XO animals, in addition to its effect on the sexual phenotype of XO animals. The epistatic relationships between tra and her genes are used to deduce a model for the action of these genes in controlling sex determination.

Major sex-determining genes and the control of sexual dimorphism in Caenorhabditis elegans

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 625-637 ◽  
Author(s):  
Jonathan Hodgkin ◽  
Andrew D. Chisholm ◽  
Michael M. Shen
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Germ Line ◽  
Cell Lineage ◽  
Regulatory Genes ◽  
Nematode Caenorhabditis Elegans ◽  
X Chromosomes ◽  
The Many ◽  
Lineage Analysis

Sex determination in Caenorhabditis elegans involves a cascade of major regulatory genes connecting the primary sex determining signal, X chromosome dosage, to key switch genes, which in turn direct development along either male or female pathways. Animals with one X chromosome (XO) are male, while animals with two X chromosomes (XX) are hermaphrodite: hermaphrodite development occurs because the action of the regulatory genes is modified in the germ line so that both sperm and oocytes are made inside a completely female soma. The regulatory genes are being examined by both genetic and molecular means. We discuss how these major genes, in particular the last switch gene in the cascade, tra-1, might regulate the many different sex-specific events that occur during the development of the hermaphrodite and of the male.Key words: nematode, Caenorhabditis elegans, sex determination, sexual differentiation, cell lineage analysis.

scholarly journals The Caenorhabditis elegans gene sdc-2 controls sex determination and dosage compensation in XX animals.

Genetics ◽  
1989 ◽  
Vol 122 (3) ◽  
pp. 579-593 ◽  
Author(s):  
C Nusbaum ◽  
B J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Apparent Effect ◽  
Linked Gene ◽  
Male Development ◽  
Coordinate Control

Abstract We have identified a new X-linked gene, sdc-2, that controls the hermaphrodite (XX) modes of both sex determination and X chromosome dosage compensation in Caenorhabditis elegans. Mutations in sdc-2 cause phenotypes that appear to result from a shift of both the sex determination and dosage compensation processes in XX animals to the XO modes of expression. Twenty-eight independent sdc-2 mutations have no apparent effect in XO animals, but cause two distinct phenotypes in XX animals: masculinization, reflecting a defect in sex determination, and lethality or dumpiness, reflecting a disruption in dosage compensation. The dosage compensation defect can be demonstrated directly by showing that sdc-2 mutations cause elevated levels of several X-linked transcripts in XX but not XO animals. While the masculinization is blocked by mutations in sex determining genes required for male development (her-1 and fem-3), the lethality, dumpiness and overexpression of X-linked genes are not, indicating that the effect of sdc-2 mutations on sex determination and dosage compensation are ultimately implemented by two independent pathways. We propose a model in which sdc-2 is involved in the coordinate control of both sex determination and dosage compensation in XX animals and acts in the regulatory hierarchy at a step prior to the divergence of the two pathways.

Genetic Analysis of X-Chromosome Dosage Compensation in Caenorhabditis elegans

Genetics ◽  
1987 ◽  
Vol 117 (1) ◽  
pp. 25-41
Author(s):  
Philip M Meneely ◽  
William B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Normal Function ◽  
Complete Loss ◽  
Loss Of Function ◽  
Recessive Mutations ◽  
Genetic Assay

ABSTRACT We have shown that the phenotypes resulting from hypomorphic mutations (causing reduction but not complete loss of function) in two X-linked genes can be used as a genetic assay for X-chromosome dosage compensation in Caenorhabditis elegans between males (XO) and hermaphrodites (XX). In addition we show that recessive mutations in two autosomal genes, dpy-21 V and dpy-26 IV, suppress the phenotypes resulting from the X-linked hypomorphic mutations, but not the phenotypes resulting from comparable autosomal hypomorphic mutations. This result strongly suggests that the dpy-21 and dpy-26 mutations cause increased X expression, implying that the normal function of these genes may be to lower the expression of X-linked genes. Recessive mutations in two other dpy genes, dpy-22 X and dpy-23 X, increase the severity of phenotypes resulting from some X-linked hypomorphic mutations, although dpy-23 may affect the phenotypes resulting from the autosomal hypomorphs as well. The mutations in all four of the dpy genes show their effects in both XO and XX animals, although to different degrees. Mutations in 18 other dpy genes do not show these effects.

Identification of X chromosome regions in Caenorhabditis elegans that contain sex-determination signal elements.

Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1105-1125
Author(s):  
C C Akerib ◽  
B J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
X Chromosomes ◽  
Sensitive Region ◽  
Signal Element ◽  
Number Of Genes ◽  
Mutant Phenotypes ◽  
Chromosome Regions

Abstract The primary sex-determination signal of Caenorhabditis elegans is the ratio of X chromosomes to sets of autosomes (X/A ratio). This signal coordinately controls both sex determination and X chromosome dosage compensation. To delineate regions of X that contain counted signal elements, we examined the effect on the X/A ratio of changing the dose of specific regions of X, using duplications in XO animals and deficiencies in XX animals. Based on the mutant phenotypes of genes that are controlled by the signal, we expected that increases (in males) or decreases (in hermaphrodites) in the dose of X chromosome elements could cause sex-specific lethality. We isolated duplications and deficiencies of specific X chromosome regions, using strategies that would permit their recovery regardless of whether they affect the signal. We identified a dose-sensitive region at the left end of X that contains X chromosome signal elements. XX hermaphrodites with only one dose of this region have sex determination and dosage compensation defects, and XO males with two doses are more severely affected and die. The hermaphrodite defects are suppressed by a downstream mutation that forces all animals into the XX mode of sex determination and dosage compensation. The male lethality is suppressed by mutations that force all animals into the XO mode of both processes. We were able to subdivide this region into three smaller regions, each of which contains at least one signal element. We propose that the X chromosome component of the sex-determination signal is the dose of a relatively small number of genes.

scholarly journals Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 119-127
Author(s):  
S A Broverman ◽  
P M Meneely
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Map ◽  
X Chromosome ◽  
Recessive Mutations ◽  
Feature Characteristic ◽  
Comparable Effect ◽  
Chromosome Recombination ◽  
The Right ◽  
Chromosome Nondisjunction ◽  
Pairing Region

Abstract Recessive mutations in three autosomal genes, him-1, him-5 and him-8, cause high levels of X chromosome nondisjunction in hermaphrodites of Caenorhabditis elegans, with no comparable effect on autosomal disjunction. Each of the mutants has reduced levels of X chromosome recombination, correlating with the increase in nondisjunction. However, normal or elevated levels of recombination occur at the end of the X chromosome hypothesized to contain the pairing region (the left end), with recombination levels decreasing in regions approaching the right end. Thus, both the number and the distribution of X chromosome exchange events are altered in these mutants. As a result, the genetic map of the X chromosome in the him mutants exhibits a clustering of genes due to reduced recombination, a feature characteristic of the genetic map of the autosomes in non-mutant animals. We hypothesize that these him genes are needed for some processive event that initiates near the left end of the X chromosome.

Microinjected DNA from the X chromosome affects sex determination in Caenorhabditis elegans

Science ◽  
1988 ◽  
Vol 242 (4882) ◽  
pp. 1146-1151 ◽  
Author(s):  
W. McCoubrey ◽  
K. Nordstrom ◽  
P. Meneely
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome

scholarly journals pag-3, a Caenorhabditis elegans Gene Involved in Touch Neuron Gene Expression and Coordinated Movement

Genetics ◽  
1996 ◽  
Vol 142 (1) ◽  
pp. 141-147 ◽  
Author(s):  
Yiwen Jia ◽  
Guofeng Xie ◽  
Eric Aamodt
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Ectopic Expression ◽  
Immunofluorescence Staining ◽  
Wild Type ◽  
Recessive Mutations ◽  
The Right ◽  
Three Factor

Mutations in a newly identified gene, pag-3, cause ectopic expression of touch neuron genes mec-7, mec-7lacZ and mec-4lacZ in the lineal sisters of the ALM touch neurons, the BDU neurons. pag-3 mutants also show a reverse kinker uncoordinated phenotype. The first pag-3 allele was isolated in a screen for mutants with altered immunofluorescence staining patterns. Two additional pag-3 alleles were identified in a noncomplementation screen of 38,000 haploid genomes. All of the pag-3 alleles were recessive to wild type and cause the same phenotypes. Two-factor crosses, deficiency mapping and three-factor crosses located pag-3 to the right arm of the X chromosome between unc-3 and unc-7. Because recessive mutations in pag-3 result in expression of several touch cell specific genes in the BDU neurons, pag-3(+) must directly or indirectly suppress expression of these genes in the BDU neurons. Although pag-3 mutants did not show mec-3lacZ expression in their BDU neurons, expression of mec-7lacZ and mec-4lacZ in the BDU neurons of pag-3 mutants required mec-3(+).

scholarly journals The dpy-30 gene encodes an essential component of the Caenorhabditis elegans dosage compensation machinery.

Genetics ◽  
1994 ◽  
Vol 137 (4) ◽  
pp. 999-1018 ◽  
Author(s):  
D R Hsu ◽  
B J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
The Other ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
General Role ◽  
Essential Component

Abstract The need to regulate X chromosome expression in Caenorhabditis elegans arises as a consequence of the primary sex-determining signal, the X/A ratio (the ratio of X chromosomes to sets of autosomes), which directs 1X@A animals to develop as males and 2X/2A animals to develop as hermaphrodites. C. elegans possesses a dosage compensation mechanism that equalizes X chromosome expression between the two sexes despite their disparity in X chromosome dosage. Previous genetic analysis led to the identification of four autosomal genes, dpy-21, dpy-26, dpy-27 and dpy-28, whose products are essential in XX animals for proper dosage compensation, but not for sex determination. We report the identification and characterization of dpy-30, an essential component of the dosage compensation machinery. Putative null mutations in dpy-30 disrupt dosage compensation and cause a severe maternal-effect, XX-specific lethality. Rare survivors of the dpy-30 lethality are dumpy and express their X-linked genes at higher than wild-type levels. These dpy-30 mutant phenotypes superficially resemble those caused by mutations in dpy-26, dpy-27 and dpy-28; however, detailed phenotypic analysis reveals important differences that distinguish dpy-30 from these genes. In contrast to the XX-specific lethality caused by mutations in the other dpy genes, the XX-specific lethality caused by dpy-30 mutations is completely penetrant and temperature sensitive. In addition, unlike the other genes, dpy-30 is required for the normal development of XO animals. Although dpy-30 mutations do not significantly affect the viability of XO animals, they do cause them to be developmentally delayed and to possess numerous morphological and behavioral abnormalities. Finally, dpy-30 mutations can dramatically influence the choice of sexual fate in animals with an ambiguous sexual identity, despite having no apparent effect on the sexual phenotype of otherwise wild-type animals. Paradoxically, depending on the genetic background, dpy-30 mutations cause either masculinization or feminization, thus revealing the complex regulatory relationship between the sex determination and dosage compensation processes. The novel phenotypes caused by dpy-30 mutations suggest that in addition to acting in the dosage compensation process, dpy-30 may play a more general role in the development of both XX and XO animals.

scholarly journals X chromosome duplications affect a region of the chromosome they do not duplicate in Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 119 (2) ◽  
pp. 365-375
Author(s):  
P M Meneely ◽  
K D Nordstrom
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Linked Gene ◽  
Hypomorphic Mutation ◽  
Level Of Activity

Abstract X chromosome duplications have been used previously to vary the dose of specific regions of the X chromosome to study dosage compensation and sex determination in Caenorhabditis elegans. We show here that duplications suppress and X-linked hypomorphic mutation and elevate the level of activity of an X-linked enzyme, although these two genes are located in a region of the X chromosome that is not duplicated. The effects do not depend on the region of the X chromosome duplicated and is stronger in strains with two doses of a duplication than in strains with one dose. This is evidence for a general elevation of X-linked gene expression in strains carrying X-chromosome duplications, consistent with the hypothesis that the duplications titrate a repressor acting on many X-linked genes.

Identification of a candidate primary sex determination locus, fox-1, on the X chromosome of Caenorhabditis elegans

Development ◽  
1994 ◽  
Vol 120 (12) ◽  
pp. 3681-3689 ◽  
Author(s):  
J. Hodgkin ◽  
J.D. Zellan ◽  
D.G. Albertson
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromosome Number ◽  
Sex Determination ◽  
X Chromosome ◽  
Cdna Clone ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Transgenic Lines ◽  
Genetic Results

Sex in Caenorhabditis elegans (XX hermaphrodite, XO male) is determined by the X:A ratio, which is the ratio of X chromosome number to autosomal set number. Recent genetic results with X chromosome duplications have suggested that there may be only a small number of major numerator sites on the X chromosome that contribute to this ratio. Mapping of duplication endpoints delimited a region of less than 300 kb, likely to contain one such element. Cosmid clones from this region were tested for numerator activity by constructing transgenic lines carrying extra copies of each tested cosmid. Most cosmid arrays have no effect on the viability of either XX or XO animals. One cosmid array was found to be viable in XX animals, but lethal and feminizing in XO animals, consistent with it containing a major numerator element. Further experiments defined a region of 12–30 kb with apparent numerator activity, which is designated fox-1, ‘Feminizing locus On X’. A cDNA clone hybridizing across part of this region encodes a predicted RNA-binding protein.

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