scholarly journals X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation

2019 ◽  
Vol 51 (2) ◽  
pp. 192-207.e6 ◽  
Author(s):  
Erika C. Anderson ◽  
Phillip A. Frankino ◽  
Ryo Higuchi-Sanabria ◽  
Qiming Yang ◽  
Qian Bian ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Domain Architecture

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 The Caenorhabditis elegans Dosage Compensation Machinery Is Recruited to X Chromosome DNA Attached to an Autosome

Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1603-1621
Author(s):  
Jason D Lieb ◽  
Carlos Ortiz de Solorzano ◽  
Enrique Garcia Rodriguez ◽  
Arthur Jones ◽  
Michael Angelo ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Dna Sequences ◽  
Three Dimensional ◽  
Dosage Compensation Complex ◽  
X Chromosomes ◽  
Cis Acting ◽  
Recognition Elements ◽  
The Right

Abstract The dosage compensation machinery of Caenorhabditis elegans is targeted specifically to the X chromosomes of hermaphrodites (XX) to reduce gene expression by half. Many of the trans-acting factors that direct the dosage compensation machinery to X have been identified, but none of the proposed cis-acting X chromosome-recognition elements needed to recruit dosage compensation components have been found. To study X chromosome recognition, we explored whether portions of an X chromosome attached to an autosome are competent to bind the C. elegans dosage compensation complex (DCC). To do so, we devised a three-dimensional in situ approach that allowed us to compare the volume, position, and number of chromosomal and subchromosomal bodies bound by the dosage compensation machinery in wild-type XX nuclei and XX nuclei carrying an X duplication. The dosage compensation complex was found to associate with a duplication of the right 30% of X, but the complex did not spread onto adjacent autosomal sequences. This result indicates that all the information required to specify X chromosome identity resides on the duplication and that the dosage compensation machinery can localize to a site distinct from the full-length hermaphrodite X chromosome. In contrast, smaller duplications of other regions of X appeared to not support localization of the DCC. In a separate effort to identify cis-acting X recognition elements, we used a computational approach to analyze genomic DNA sequences for the presence of short motifs that were abundant and overrepresented on X relative to autosomes. Fourteen families of X-enriched motifs were discovered and mapped onto the X chromosome.

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 Molecular analysis of X chromosome dosage compensation in Caenorhabditis elegans.

1987 ◽  
Vol 84 (21) ◽  
pp. 7600-7604 ◽  
Author(s):  
L. M. Donahue ◽  
B. A. Quarantillo ◽  
W. B. Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Molecular Analysis ◽  
X Chromosome ◽  
Dosage Compensation

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.

scholarly journals Two Classes of Dosage Compensation Complex Binding Elements along Caenorhabditis elegans X Chromosomes

2009 ◽  
Vol 29 (8) ◽  
pp. 2023-2031 ◽  
Author(s):  
Timothy A. Blauwkamp ◽  
Gyorgyi Csankovszki
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Gene Products ◽  
Dosage Compensation Complex ◽  
X Chromosomes ◽  
Linked Gene ◽  
Unknown Mechanism

ABSTRACT Dosage compensation equalizes X-linked gene products between the sexes. In Caenorhabditis elegans, the dosage compensation complex (DCC) binds both X chromosomes in XX animals and halves the transcription from each. The DCC is recruited to the X chromosomes by a number of loci, rex sites, and is thought to spread from these sites by an unknown mechanism to cover the rest of the chromosome. Here we describe a novel class of DCC-binding elements that we propose serve as “way stations” for DCC binding and spreading. Both rex sites and way stations comprise strong foci of DCC binding on the native X chromosome. However, rex sites maintain their ability to bind large amounts of DCC even on X duplications detached from the native X, while way stations do not. These results suggest that two distinct classes of DCC-binding elements facilitate recruitment and spreading of the DCC along the X chromosome.

scholarly journals Assessment of X Chromosome Dosage Compensation in Caenorhabditis elegans by Phenotypic Analysis of lin-14

Genetics ◽  
1987 ◽  
Vol 117 (4) ◽  
pp. 657-670
Author(s):  
Leslie DeLong ◽  
Lawrence P Casson ◽  
Barbara J Meyer
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Phenotypic Expression ◽  
Transcript Level ◽  
Phenotypic Analysis ◽  
Linked Gene ◽  
Chromosome Gene ◽  
The Difference

ABSTRACT Caenorhabditis elegans compensates for the difference in X chromosome gene dose between males (XO) and hermaphrodites (XX) through a mechanism that equalizes the levels of X-specific mRNA transcripts between the two sexes. We have devised a sensitive and quantitative genetic assay to measure perturbations in X chromosome gene expression caused by mutations that affect this process of dosage compensation. The assay is based on quantitating the precocious alae phenotype caused by a mutation that reduces but does not eliminate the function of the X-linked gene lin-14. We demonstrate that in diploid animals the lin-14 gene is dosage compensated between XO and XX animals. In XXX diploid animals, however, lin-14 expression is not compensated, implying that the normal dosage compensation mechanism in C. elegans lacks the capacity to compensate completely for the additional X chromosome in triplex animals. Using the lin-14 assay we compare the effects of mutations in the genes dpy-21, dpy-26, dpy-27, dpy-28, and dpy-22 on X-linked gene expression. Additionally, in the case of dpy-21 we correlate the change in phenotypic expression of lin-14 with a corresponding change in the lin-14 mRNA transcript level.

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