The
            <i>Caenorhabditis elegans</i>
            maternal-effect sterile proteins, MES-2, MES-3, and MES-6, are associated in a complex in embryos

Xu, Lei; Fong, Youyi; Strome, Susan

doi:10.1073/pnas.081016198

Cited by 66 publications

(66 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Strong genetic and biochemical evidence indicates that the MES-2-MES-3-MES-6 complex is functionally analogous to the PRC2 complex (Xu et al, 2001a), which places the histone H3K27me3 mark characteristic of Polycomb repression (Bender et al, 2004;Fong et al, 2002;Holdeman et al, 1998;Xu et al, 2001a (Wang et al, 2004a;Yang et al, 2007;Zhang et al, 2003;Zhang et al, 2004). All are essential genes, and mutants carrying partial loss-of-function alleles have severe defects not observed in mes null mutants, suggesting that the sop and sor genes have many important functions in somatic cells and do not simply maintain the pattern of gene expression established by the mes genes, which have subtle functions in somatic cells (Ross and Zarkower, 2003).…”

Section: Discussionmentioning

confidence: 99%

MIG-32 and SPAT-3A are PRC1 homologs that control neuronal migration inCaenorhabditis elegans

2009

View full text Add to dashboard Cite

The Polycomb repression complex 2 (PRC2) methylates histone H3 lysine 27 at target genes to modify gene expression, and this mark is recognized by PRC1, which ubiquitylates histone H2A. In Caenorhabditis elegans, a complex of the MES-2, MES-3 and MES-6 proteins is functionally analogous to the PRC2 complex, but the functional analog of PRC1, and indeed whether C. elegans has such a complex, has been unclear. We describe here that MIG-32 and SPAT-3A are functional analogs of PRC1 in C. elegans, where they are required for neuronal migrations and during vulval development. mig-32 and spat-3 mutants are defective in H2A ubiquitylation, and have nervous system defects that partially overlap with those of mes mutants. However, unlike the mes mutants, mig-32 and spat-3 mutants are fertile, suggesting that PRC1 function is not absolutely required in the germline for essential functions of PRC2.

show abstract

Section: Discussionmentioning

confidence: 99%

MIG-32 and SPAT-3A are PRC1 homologs that control neuronal migration inCaenorhabditis elegans

2009

View full text Add to dashboard Cite

show abstract

“…6A). Thus, the ϳ255-kDa MES complex detected in worm embryos (68), which is close in size to the sum of the three MES proteins (ϳ230 kDa), likely represents an enzymatically active complex consisting solely of these components.…”

Section: Fig 4 Effects Of Esc Mutations On Assembly and Hmtase Actimentioning

confidence: 99%

“…The E(Z) homolog, MES-2, and the ESC homolog, MES-6, are subunits in a worm MES complex that is required for germ line development and gene silencing (13,17,21,25,68) and also plays a role in Hox gene repression in the soma (46). Besides MES-2 and MES-6, the MES complex contains MES-3, which is a novel protein unrelated to PcG proteins from other species.…”

mentioning

confidence: 99%

Subunit Contributions to Histone Methyltransferase Activities of Fly and Worm Polycomb Group Complexes

Ketel

Andersen

Vargas

et al. 2005

Molecular and Cellular Biology

Self Cite

181

196

View full text Add to dashboard Cite

The ESC-E(Z) complex of Drosophila melanogaster Polycomb group (PcG) repressors is a histone H3 methyltransferase (HMTase). This complex silences fly Hox genes, and related HMTases control germ line development in worms, flowering in plants, and X inactivation in mammals. The fly complex contains a catalytic SET domain subunit, E(Z), plus three noncatalytic subunits, SU(Z)12, ESC, and NURF-55. The four-subunit complex is >1,000-fold more active than E(Z) alone. Here we show that ESC and SU(Z)12 play key roles in potentiating E(Z) HMTase activity. We also show that loss of ESC disrupts global methylation of histone H3-lysine 27 in fly embryos. Subunit mutations identify domains required for catalytic activity and/or binding to specific partners. We describe missense mutations in surface loops of ESC, in the CXC domain of E(Z), and in the conserved VEFS domain of SU(Z)12, which each disrupt HMTase activity but preserve complex assembly. Thus, the E(Z) SET domain requires multiple partner inputs to produce active HMTase. We also find that a recombinant worm complex containing the E(Z) homolog, MES-2, has robust HMTase activity, which depends upon both MES-6, an ESC homolog, and MES-3, a pioneer protein. Thus, although the fly and mammalian PcG complexes absolutely require SU(Z)12, the worm complex generates HMTase activity from a distinct partner set.

show abstract

“…For example, mes-6 and cgh-1 are both required in the germline and are expressed slightly more in hermaphrodites. mes-6 is a member of the Polycomb-like chromatin repressive complex (Xu et al 2001) and cgh-1 inhibits apoptosis in oocytes (Navarro et al 2001). Consistent with the idea that sex-biased expression correlates with sex-biased roles, we find that genes with sex-biased expression are enriched for reproductive and neuronal functions (Table 2), while genes that are dosage compensated are known to be important in both sexes ( Figure 4C).…”

Section: Discussionmentioning

confidence: 99%

Untangling the Contributions of Sex-Specific Gene Regulation and X-Chromosome Dosage to Sex-Biased Gene Expression in Caenorhabditis elegans

Kramer¹,

Rao²,

Ercan

2016

Genetics

View full text Add to dashboard Cite

Dosage compensation mechanisms equalize the level of X chromosome expression between sexes. Yet the X chromosome is often enriched for genes exhibiting sex-biased, i.e., imbalanced expression. The relationship between X chromosome dosage compensation and sex-biased gene expression remains largely unexplored. Most studies determine sex-biased gene expression without distinguishing between contributions from X chromosome copy number (dose) and the animal's sex. Here, we uncoupled X chromosome dose from sex-specific gene regulation in Caenorhabditis elegans to determine the effect of each on X expression. In early embryogenesis, when dosage compensation is not yet fully active, X chromosome dose drives the hermaphrodite-biased expression of many X-linked genes, including several genes that were shown to be responsible for hermaphrodite fate. A similar effect is seen in the C. elegans germline, where X chromosome dose contributes to higher hermaphrodite X expression, suggesting that lack of dosage compensation in the germline may have a role in supporting higher expression of X chromosomal genes with female-biased functions in the gonad. In the soma, dosage compensation effectively balances X expression between the sexes. As a result, somatic sex-biased expression is almost entirely due to sex-specific gene regulation. These results suggest that lack of dosage compensation in different tissues and developmental stages allow X chromosome copy number to contribute to sex-biased gene expression and function.KEYWORDS dosage compensation; C. elegans; RNA-seq; sex; sex-biased gene expression; chromatin; X chromosome; transcription; gene regulation; germline; XO; genetics of sex M ALES and females exhibit many phenotypic differences, termed sexual dimorphisms. With the exception of the gene-poor Y chromosome, the two sexes share identical genomes. Thus, sexual dimorphisms stem from differences in gene expression between sexes. Genes that are expressed differently between sexes include those expressed exclusively (sex specific) or at a higher level in one sex (sex biased). Sexbiased expression allows a gene to be more active in the sex that it benefits without a potential cost to the opposite sex. Sex-biased gene expression is common throughout metazoans. Previous studies indicate up to 60% of all genes show sex-biased expression [in mice (Khil et al. 2004;Yang et al. 2006;Reinius et al. 2012), flies (Parisi et al. 2003;Ranz et al. 2003;Allen et al. 2013;Kaiser and Bachtrog 2014), and nematodes (Reinke et al. 2004;Thomas et al. 2012;Albritton et al. 2014)].Previous genome-wide studies found that compared to autosomes, the X chromosome generally harbors more genes with female-biased expression and fewer genes with malebiased expression [in mice (Khil et al. 2004;Yang et al. 2006;Reinius et al. 2012), flies (Parisi et al. 2003;Ranz et al. 2003), and nematodes (Reinke et al. 2004;Thomas et al. 2012;Albritton et al. 2014)]. However, this observed enrichment of female bias and depletion of male bias from the X is a gene...

show abstract

The Caenorhabditis elegans maternal-effect sterile proteins, MES-2, MES-3, and MES-6, are associated in a complex in embryos

Abstract: The Caenorhabditis elegans maternal-effect sterile genes, mes-2, mes-3, mes-4, and mes-6, encode nuclear proteins that are essential for germ-line development. They are thought to be involved in a common process because their mutant phenotypes are similar.

Cited by 66 publications

References 43 publications

MIG-32 and SPAT-3A are PRC1 homologs that control neuronal migration inCaenorhabditis elegans

MIG-32 and SPAT-3A are PRC1 homologs that control neuronal migration inCaenorhabditis elegans

Subunit Contributions to Histone Methyltransferase Activities of Fly and Worm Polycomb Group Complexes

Untangling the Contributions of Sex-Specific Gene Regulation and X-Chromosome Dosage to Sex-Biased Gene Expression in Caenorhabditis elegans

Contact Info

Product

Resources

About