scholarly journals The Primary Sex Determination Signal of Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 152 (3) ◽  
pp. 999-1015 ◽  
Author(s):  
Ilil Carmi ◽  
Barbara J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Counting Process ◽  
Rna Binding ◽  
Nuclear Hormone Receptor ◽  
Chromosome Counting ◽  
Specific Expression ◽  
X Chromosomes ◽  
Signal Element ◽  
Complete Transformation

AbstractAn X chromosome counting process determines sex in Caenorhabditis elegans. The dose of X chromosomes is translated into sexual fate by a set of X-linked genes that together control the activity of the sex-determination and dosage-compensation switch gene, xol-1. The double dose of X elements in XX animals represses xol-1 expression, promoting the hermaphrodite fate, while the single dose of X elements in XO animals permits high xol-1 expression, promoting the male fate. Previous work has revealed at least four signal elements that repress xol-1 expression at two levels, transcriptional and post-transcriptional. The two molecularly characterized elements include an RNA binding protein and a nuclear hormone receptor homolog. Here we explore the roles of the two mechanisms of xol-1 repression and further investigate how the combined dose of X signal elements ensures correct, sex-specific expression of xol-1. By studying the effects of increases and decreases in X signal element dose on male and hermaphrodite fate, we demonstrate that signal elements repress xol-1 cumulatively, such that full repression of xol-1 in XX animals results from the combined effect of individual elements. Complete transformation from the hermaphrodite to the male fate requires a decrease in the dose of all four elements, from two copies to one. We show that both mechanisms of xol-1 repression are essential and act synergistically to keep xol-1 levels low in XX animals. However, increasing repression by one mechanism can compensate for loss of the other, demonstrating that each mechanism can exert significant xol-1 repression on its own. Finally, we present evidence suggesting that xol-1 activity can be set at intermediate levels in response to an intermediate X signal.

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.

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 DM Domain Transcription Factor MAB-3 Regulates Male Hypersensitivity to Oxidative Stress in Caenorhabditis elegans

2010 ◽  
Vol 30 (14) ◽  
pp. 3453-3459 ◽  
Author(s):  
Hideki Inoue ◽  
Eisuke Nishida
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Target Genes ◽  
Stress Sensitivity ◽  
Gata Factor ◽  
X Chromosomes ◽  
C Elegans ◽  
Dm Domain

ABSTRACT Sex differences occur in most species and involve a variety of biological characteristics. The nematode Caenorhabditis elegans consists of two sexes, self-fertile hermaphrodites (XX) and males (XO). Males differ from hermaphrodites in morphology, behavior, and life span. Here, we find that male C. elegans worms are much more sensitive than hermaphrodites to oxidative stress and show that the DM domain transcription factor MAB-3 plays a pivotal role in determining this male hypersensitivity. The hypersensitivity to oxidative stress does not depend on the dosage of X chromosomes but is determined by the somatic sex determination pathway. Our analyses show that the male hypersensitivity is controlled by MAB-3, one of the downstream effectors of the master terminal switch TRA-1 in the sex determination pathway. Moreover, we find that MAB-3 suppresses expression of several transcriptional target genes of the ELT-2 GATA factor, which is a global regulator of transcription in the C. elegans intestine, and show that RNA interference (RNAi) against elt-2 increases sensitivity to oxidative stress. These results strongly suggest that the DM domain protein MAB-3 regulates oxidative stress sensitivity by repressing transcription of ELT-2 target genes in the intestine.

scholarly journals Distinct developmental mechanisms influence sexual dimorphisms in the milkweed bug Oncopeltus fasciatus

2021 ◽  
Author(s):  
Josefine Just ◽  
Mara Laslo ◽  
Ye Jin Lee ◽  
Michael C Yarnell ◽  
Zhuofan Zhang ◽  
...  
Keyword(s):  
Sex Determination ◽  
The Body ◽  
Oncopeltus Fasciatus ◽  
Sexually Dimorphic ◽  
Specific Expression ◽  
X Chromosomes ◽  
Milkweed Bug ◽  
Multiple Transcripts ◽  
Complex Protein ◽  
Male Specific

Sexual dimorphism is a common feature of animals. Sex determination mechanisms vary widely among species and evolve rapidly. Until recently studies have found consistent mechanisms across the body of each individual determine female or male dimorphic body structures. In sexually dimorphic cells throughout the body of Drosophila, the relative dosage of autosomes and X chromosomes leads indirectly to alternatively spliced transcripts from the gene doublesex. The female Dsx isoform interacts with the mediator complex protein encoded by intersex to activate female development in flies. In males the transcription factor encoded by fruitless promotes male-specific behavior. In the milkweed bug Oncopeltus fasciatus, we find a requirement for different combinations of these genes during development of distinct dimorphic structures, within the same sex, suggesting a previously unappreciated level of diversity in sex determination. While intersex and fruitless are structurally conserved, doublesex has a history of duplication and divergence among Paraneoptera. Three doublesex paralogs in O. fasciatus produce multiple transcripts with sex- and tissue-specific expression. intersex and fruitless are expressed across the body, in females and males. RNA interference reveals only one doublesex paralog functions in somatic sex determination. Knockdown of doublesex and fruitless produces intersex phenotypic conditions in two sexually dimorphic structures: genitalia and abdominal sternites. In contrast, intersex is required for dimorphic development of female and male genitalia, but not for sternite dimorphism. These results reveal sex determination roles for intersex and fruitless distinct from their orthologs in other insects. Our results illuminate a novel form of developmental diversity in insect sex determination.

scholarly journals sisterless A is required for the activation of Sex lethal in the germline

2019 ◽  
Author(s):  
Raghav Goyal ◽  
Ellen Baxter ◽  
Mark Van Doren
Keyword(s):  
Sex Determination ◽  
X Chromosome ◽  
Germ Cells ◽  
Specific Expression ◽  
Male Germ Cells ◽  
X Chromosomes ◽  
Dna Elements ◽  
Sex Lethal ◽  
Female Specific ◽  
Necessary And Sufficient

ABSTRACTIn Drosophila, sex determination in somatic cells has been well-studied and is under the control of the switch gene Sex lethal (Sxl), which is activated in females by the presence of two X chromosomes. Though sex determination is regulated differently in the germline versus the soma, Sxl is also necessary and sufficient for the female identity in germ cells. Loss of Sxl function in the germline results in ovarian germline tumors, a characteristic of male germ cells developing in a female soma. Further, XY (male) germ cells expressing Sxl are able to produce eggs when transplanted into XX (female) somatic gonads, demonstrating that Sxl is also sufficient for female sexual identity in the germline. As in the soma, the presence of two X chromosomes is sufficient to activate Sxl in the germline, but the mechanism for “counting” X chromosomes in the germline is thought to be different from the soma. Here we have explored this mechanism at both cis- and trans-levels. Our data support the model that the Sxl “establishment” promoter (SxlPE) is activated in a female-specific manner in the germline, as in the soma, but that the timing of SxlPE activation, and the DNA elements that regulate SxlPE are different from those in the soma. Nevertheless, we find that the X chromosome-encoded gene sisterless A (sisA), which helps activate Sxl in the soma, is also essential for Sxl activation in the germline. Loss of sisA function leads to loss of Sxl expression in the germline, and to ovarian tumors and germline loss. These defects can be rescued by the expression of Sxl, demonstrating that sisA lies upstream of Sxl in germline sex determination. We conclude that sisA acts as an X chromosome counting element in both the soma and the germline, but that additional factors that ensure robust, female-specific expression of Sxl in the germline remain to be discovered.

Genetics of sex determination: what can we learn from Drosophila?

Development ◽  
1987 ◽  
Vol 101 (Supplement) ◽  
pp. 17-24
Author(s):  
Rolf Nöthiger ◽  
Monica Steinmann-Zwicky
Keyword(s):  
Molecular Biology ◽  
Sex Determination ◽  
Genetic Control ◽  
Sexual Development ◽  
Sexual Differentiation ◽  
Regulatory Elements ◽  
Negative Control ◽  
Homeotic Genes ◽  
Specific Expression ◽  
X Chromosomes

The combined efforts of genetics, developmental and molecular biology have revealed the principles of genetic control of sexual differentiation in Drosophila. In combination with maternal components, a quantitative chromosomal signal, provided by the ratio of X chromosomes to sets of autosomes (X: A), regulates a key gene (Sxl). The functional state, ON or OFF, of Sxl, via a few subordinate regulatory genes, controls a switch gene (dsx) that can express two mutually exclusive functions, M or F. These serve to repress either the female or the male set of differentiation genes, thus directing the cells either into the male or into the female sexual pathway. Investigations of control genes and their regulation show that they have properties of homeotic genes. Their role is to select one of two alternative developmental programs. Their function, or lack of function, is required throughout development to maintain the cells in their respective sexual pathway. Differentiation genes are under negative control by dsx. We discuss the cis- and tams-regulatory elements that are needed for sex-, tissue- and stage-specific expression of the differentiation genes. A comparison of Drosophila to other organisms such as Caenorhabditis, mammals and other insects indicates similarities that we interpret as evidence for a basically invariant genetic strategy used by various organisms to regulate sexual development.

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.

scholarly journals Isolation of dominant XO-feminizing mutations in Caenorhabditis elegans: new regulatory tra alleles and an X chromosome duplication with implications for primary sex determination.

Genetics ◽  
1995 ◽  
Vol 141 (2) ◽  
pp. 527-542
Author(s):  
J Hodgkin ◽  
D G Albertson
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Chemical Mutagenesis ◽  
The Novel ◽  
X Chromosomes ◽  
Inverted Orientation ◽  
Fertile Female ◽  
Fertile Male ◽  
Selection Of

Abstract A strain of Caenorhabditis elegans was constructed that permits selection of dominant or sex-linked mutations that transform XO animals (normally male) into fertile females, using a feminizing mutation, tra-2(e2046gf), which by itself does not sexually transform XO males. Twenty-three mutations were isolated after chemical mutagenesis and found to fall into both expected classes (four dominant tra-1 mutations and eight recessive xol-1 mutations) and novel classes. The novel mutations include 10 second-site mutations of tra-2, which are called eg mutations, for enhanced gain-of-function. The tra-2(gf, eg) alleles lead to complete dominant transformation of XO animals from fertile male into fertile female. Also isolated was a duplication of the left end of the X chromosome, eDp26, which has dominant XO lethal and feminizing properties, unlike all previously isolated duplications of the X chromosome. The properties of eDp26 indicate that it carries copies of one or more numerator elements, which act as part of the primary sex-determination signal, the X:A ratio. The eDp26 duplication is attached to the left tip of the X chromosome in inverted orientation and consequently can be used to generate unstable attached-X chromosomes.

scholarly journals Sperm fate is promoted by the mir-44 microRNA family in the Caenorhabditis elegans hermaphrodite germline

Genetics ◽  
2020 ◽  
Vol 217 (1) ◽  
Author(s):  
Katherine A Maniates ◽  
Benjamin S Olson ◽  
Allison L Abbott
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Larval Development ◽  
Cell Fate ◽  
Rna Binding ◽  
Regulation Of Gene Expression ◽  
Cell Fate Decisions ◽  
Normal Period ◽  
Germline Sex Determination

Abstract Posttranscriptional regulation of gene expression, typically effected by RNA-binding proteins, microRNAs (miRNAs), and translation initiation factors, is essential for normal germ cell function. Numerous miRNAs have been detected in the germline; however, the functions of specific miRNAs remain largely unknown. Functions of miRNAs have been difficult to determine as miRNAs often modestly repress target mRNAs and are suggested to sculpt or fine tune gene expression to allow for the robust expression of cell fates. In Caenorhabditis elegans hermaphrodites, cell fate decisions are made for germline sex determination during larval development when sperm are generated in a short window before the switch to oocyte production. Here, analysis of newly generated mir-44 family mutants has identified a family of miRNAs that modulate the germline sex determination pathway in C. elegans. Mutants with the loss of mir-44 and mir-45 produce fewer sperm, showing both a delay in the specification and formation of sperm as well as an early termination of sperm specification accompanied by a premature switch to oocyte production. mir-44 and mir-45 are necessary for the normal period of fog-1 expression in larval development. Through genetic analysis, we find that mir-44 and mir-45 may act upstream of fbf-1 and fem-3 to promote sperm specification. Our research indicates that the mir-44 family promotes sperm cell fate specification during larval development and identifies an additional posttranscriptional regulator of the germline sex determination pathway.

scholarly journals Sex determination in polyploids of Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 137 (2) ◽  
pp. 467-481
Author(s):  
P M Meneely
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Dna Sequences ◽  
Maternal Effect ◽  
Indirect Evidence ◽  
Sex Reversal ◽  
Diploid Males ◽  
X Chromosomes

Abstract In Caenorhabditis elegans triploid animals with two X chromosomes (symbolized 3A;2X) are males. However, these triploid males can be feminized by making them mutant for recessive dosage compensation mutations, by adding X chromosome duplications or by microinjecting particular DNA sequences termed feminizing elements. None of these treatments affects diploid males. This study explores several aspects of these treatments in polyploids. The dosage compensation mutants exhibit a strong maternal effect, such that reduction of any of the dosage compensation gene functions in the mother leads to sex reversal of 3A;2X animals. Likewise, all X chromosome duplications tested cause both sex reversal and intersexual development of many 3A;2X animals. Microinjected feminizing element DNA does not cause extensive sex reversal, but does result in intersexual development in 3A;2X animals. Neither X chromosome duplications nor microinjected feminizing elements show that extreme maternal effect of the dosage compensation mutants, although there is indirect evidence for a maternal effect of the feminizing elements. In particular, very little feminizing element DNA needs to be microinjected in order to feminize triploid males, far less than what is needed for stable inheritance, implying that feminizing elements can work within the mother's gonad. However, even very high concentrations of microinjected feminizing elements do not affect sex determination in diploid males, suggesting that they are not part of the numerator of the X/A ratio. In addition, no pair of X chromosome duplications feminizes diploid males, suggesting that none of these duplications contains a numerator of the X/A ratio. Instead, I infer that an X-linked locus, as yet undefined, must be present in two copies for hermaphrodite development to ensue or that the two X chromosomes might interact.

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