Maternal control of a zygotic patterning gene in Caenorhabditis elegans

The transition from maternal to zygotic gene control is a key process in embryogenesis. Although many maternal effect genes have been studied in the C. elegans embryo, how their activities lead to the positional expression of zygotic patterning genes has not yet been established. Evidence is presented showing that expression of the zygotic patterning gene vab-7 does not depend on cell position or cell contacts, but rather on the production of a C blastomere. Furthermore, pal-1, a caudal homologue with maternal product necessary for the proper development of the C blastomere, is both necessary and sufficient for vab-7 expression. This provides a link between maternal gene activity and zygotic patterning gene expression in C. elegans. The results suggest that zygotic patterning genes might be generally controlled at the level of blastomere fate and not by position.

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Maternal-Zygotic Epistasis and the Evolution of Genetic Diseases

Journal of Biomedicine and Biotechnology ◽

10.1155/2010/478732 ◽

2010 ◽

Vol 2010 ◽

pp. 1-13 ◽

Cited By ~ 2

Author(s):

Nicholas K. Priest ◽

Michael J. Wade

Keyword(s):

Gene Expression ◽

Disease Susceptibility ◽

Genetic Model ◽

Genetic Diseases ◽

Epistatic Interactions ◽

High Frequencies ◽

Plausible Values ◽

Maternal Effect Genes ◽

Zygotic Gene ◽

Maternal Gene

Many birth defects and genetic diseases are expressed in individuals that do not carry the disease causing alleles. Genetic diseases observed in offspring can be caused by gene expression in mothers and by interactions between gene expression in mothers and offspring. It is not clear whether the underlying pattern of gene expression (maternal versus offspring) affects the incidence of genetic disease. Here we develop a 2-locus population genetic model with epistatic interactions between a maternal gene and a zygotic gene to address this question. We show that maternal effect genes that affect disease susceptibility in offspring persist longer and at higher frequencies in a population than offspring genes with the same effects. We find that specific forms of maternal-zygotic epistasis can maintain disease causing alleles at high frequencies over a range of plausible values. Our findings suggest that the strength and form of epistasis and the underlying pattern of gene expression may greatly influence the prevalence of human genetic diseases.

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The Polycomb group in Caenorhabditis elegans and maternal control of germline development

Development ◽

10.1242/dev.125.13.2469 ◽

1998 ◽

Vol 125 (13) ◽

pp. 2469-2478 ◽

Cited By ~ 7

Author(s):

I. Korf ◽

Y. Fan ◽

S. Strome

Keyword(s):

Gene Expression ◽

Caenorhabditis Elegans ◽

Polycomb Group ◽

Polycomb Group Proteins ◽

Polycomb Group Protein ◽

Maternal Control ◽

Germline Development ◽

C Elegans ◽

Polycomb Group Genes ◽

Group Protein

Four Caenorhabditis elegans genes, mes-2, mes-3, mes-4 and mes-6, are essential for normal proliferation and viability of the germline. Mutations in these genes cause a maternal-effect sterile (i.e. mes) or grandchildless phenotype. We report that the mes-6 gene is in an unusual operon, the second example of this type of operon in C. elegans, and encodes the nematode homolog of Extra sex combs, a WD-40 protein in the Polycomb group in Drosophila. mes-2 encodes another Polycomb group protein (see paper by Holdeman, R., Nehrt, S. and Strome, S. (1998). Development 125, 2457–2467). Consistent with the known role of Polycomb group proteins in regulating gene expression, MES-6 is a nuclear protein. It is enriched in the germline of larvae and adults and is present in all nuclei of early embryos. Molecular epistasis results predict that the MES proteins, like Polycomb group proteins in Drosophila, function as a complex to regulate gene expression. Database searches reveal that there are considerably fewer Polycomb group genes in C. elegans than in Drosophila or vertebrates, and our studies suggest that their primary function is in controlling gene expression in the germline and ensuring the survival and proliferation of that tissue.

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Neuronal cell migration in C. elegans: regulation of Hox gene expression and cell position

Development ◽

10.1242/dev.122.10.3117 ◽

1996 ◽

Vol 122 (10) ◽

pp. 3117-3131 ◽

Cited By ~ 28

Author(s):

J. Harris ◽

L. Honigberg ◽

N. Robinson ◽

C. Kenyon

Keyword(s):

Gene Expression ◽

Cell Migration ◽

Neuronal Cell ◽

Body Region ◽

Wild Type ◽

Hox Gene ◽

Anteroposterior Axis ◽

C Elegans ◽

Cell Position ◽

Posterior Body Region

In C. elegans, the Hox gene mab-5, which specifies the fates of cells in the posterior body region, has been shown to direct the migrations of certain cells within its domain of function. mab-5 expression switches on in the neuroblast QL as it migrates into the posterior body region. mab-5 activity is then required for the descendants of QL to migrate to posterior rather than anterior positions. What information activates Hox gene expression during this cell migration? How are these cells subsequently guided to their final positions? We address these questions by describing four genes, egl-20, mig-14, mig-1 and lin-17, that are required to activate expression of mab-5 during migration of the QL neuroblast. We find that two of these genes, egl-20 and mig-14, also act in a mab-5-independent way to determine the final stopping points of the migrating Q descendants. The Q descendants do not migrate toward any obvious physical targets in wild-type or mutant animals. Therefore, these genes appear to be part of a system that positions the migrating Q descendants along the anteroposterior axis.

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A microRNA family exerts maternal control on sex determination in C. elegans

10.1101/083949 ◽

2016 ◽

Cited By ~ 1

Author(s):

Katherine McJunkin ◽

Victor Ambros

Keyword(s):

Gene Expression ◽

Sex Determination ◽

Target Genes ◽

Rna Binding ◽

Sex Chromosome ◽

Rna Binding Proteins ◽

Early Embryo ◽

C Elegans ◽

Microrna Family ◽

Zygotic Gene

AbstractGene expression in early animal embryogenesis is in large part controlled post-transcriptionally. Maternally-contributed microRNAs may therefore play important roles in early development. We have elucidated a major biological role of the nematode mir-35 family of maternally-contributed, essential microRNAs. We show that this microRNA family regulates the sex determination pathway at multiple levels, acting both upstream and downstream of her-1 to prevent aberrantly activated male developmental programs in hermaphrodite embryos. The predicted target genes that act downstream of the mir-35 family in this process, sup-26 and nhl-2, both encode RNA binding proteins, thus delineating a previously unknown post-transcriptional regulatory subnetwork within the well-studied sex determination pathway of C. elegans. Genome-wide profiling of SUP-26 binding targets reveals 775 mRNAs, most of which have no known role in sex determination, suggesting that the mir-35 family may modulate numerous other pathways via regulation of sup-26. Since sex determination in C. elegans requires zygotic gene expression to read the sex chromosome karyotype, early embryos must remain gender-naïve; our findings show that the mir-35 family microRNAs act in the early embryo to function as a developmental timer that preserves naïveté and prevents premature deleterious developmental decisions.

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The Drosophila morphogenetic protein Bicoid binds DNA cooperatively

Development ◽

10.1242/dev.122.4.1195 ◽

1996 ◽

Vol 122 (4) ◽

pp. 1195-1206 ◽

Cited By ~ 7

Author(s):

X. Ma ◽

D. Yuan ◽

K. Diepold ◽

T. Scarborough ◽

J. Ma

Keyword(s):

Gene Expression ◽

Dna Binding ◽

Protein Interaction ◽

Fold Increase ◽

Enhancer Element ◽

Protein Protein Interaction ◽

Morphogenetic Protein ◽

Zygotic Gene ◽

Morphogenetic Gradient ◽

Maternal Gene

The Drosophila morphogenetic protein Bicoid, encoded by the maternal gene bicoid, is required for the development of the anterior structures in the embryo. Bicoid, a transcriptional activator containing a homeodomain, is distributed in an anterior-to-posterior gradient in the embryo. In response to this gradient, the zygotic gene hunchback is expressed uniformly in the anterior half of the embryo in a nearly all-or-none manner. In this report we demonstrate that a recombinant Bicoid protein binds cooperatively to its sites within a hunchback enhancer element. A less than 4-fold increase in Bicoid concentration is sufficient to achieve an unbound/bound transition in DNA binding. Using various biochemical and genetic methods we further demonstrate that Bicoid molecules can interact with each other. Our results are consistent with previous studies performed in the embryo, and they suggest that one mechanism to achieve a sharp on/off switch of gene expression in response to a morphogenetic gradient is cooperative DNA binding facilitated by protein-protein interaction.

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MATERNAL-ZYGOTIC LETHAL INTERACTIONS IN DROSOPHILA MELANOGASTER: THE EFFECTS OF DEFICIENCIES IN THE ZESTE-WHITE REGION OF THE X CHROMOSOME

Genetics ◽

10.1093/genetics/96.1.187 ◽

1980 ◽

Vol 96 (1) ◽

pp. 187-200 ◽

Cited By ~ 1

Author(s):

Leonard G Robbins

Keyword(s):

Gene Expression ◽

Drosophila Melanogaster ◽

X Chromosome ◽

Position Effect ◽

Gene Activity ◽

Position Effect Variegation ◽

White Region ◽

Effect Variegation ◽

Zygotic Gene ◽

Maternal Gene

ABSTRACT The possibility that essential loci in the zeste-white region of the Drosophila melanogaster X chromosome are expressed both maternally and zygotically has been tested. Maternal gene activity was varied by altering gene dose, and zygotic gene activity was manipulated by use of position-effect variegation of a duplication. Viability is affected when both maternal and zygotic gene activity are reduced, but not when either maternal or zygotic gene activity is normal. Tests of a set of overlapping deficiencies demonstrate that at least three sections of the zeste-white region yield maternal zygotic lethal interactions. Single-cistron mutations at two loci in one of these segments have been tested, and maternal heterozygosity for mutations at both loci give lethal responses of mutant-duplication zygotes. Thus, at least four of the 13 essential functions coded in the zeste-white region are active both maternally and zygotically, suggesting that a substantial fraction of the genome may function at both stages. The normal survival of zygotes when either maternal gene expression or zygotic gene expression is normal, and their inviability when both are depressed, suggests that a developmental stage exists when maternally determined functions and zygotically coded functions are both in use.

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