MEX-5 and MEX-6 Function to Establish Soma/Germline Asymmetry in Early C. elegans Embryos

Schubert, Charlotte; Lin, Rueyling; Vries, Corry J de; Plasterk, Ronald H.A.; Priess, James R

doi:10.1016/s1097-2765(00)80246-4

Cited by 234 publications

(368 citation statements)

References 48 publications

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“…Mammalian TIS11-like zinc-finger-containing proteins have been shown to function either as transcription factors or RNA-binding proteins (Taylor et al 1996;Worthington et al 2002). Several C. elegans genes encoding proteins with TIS11-like zinc-finger domains have been described, including pie-1, mex-1, pos-1, mex-5, and mex-6, all of which are involved in early blastomere cellfate determination and germline development (Mello et al 1996;Guedes and Priess 1997;Tabara et al 1999;Schubert et al 2000). In addition, the recently identified TIS11-like proteins OMA-1, OMA-2, and OMA-3 are redundantly required for prophase progression during oocyte maturation (Detwiler et al 2001;Shimada et al 2002).…”

Section: Identification Of Mutations In the C Elegans Gla-3 Genementioning

confidence: 99%

C. elegans GLA-3 is a novel component of the MAP kinase MPK-1 signaling pathway required for germ cell survival

Kritikou

Milstein²,

Vidalain³

et al. 2006

Genes Dev.

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During oocyte development in Caenorhabditis elegans, approximately half of all developing germ cells undergo apoptosis. While this process is evolutionarily conserved from worms to humans, the regulators of germ cell death are still largely unknown. In a genetic screen for novel genes involved in germline apoptosis in Caenorhabditis elegans, we identified and cloned gla-3. Loss of gla-3 function results in increased germline apoptosis and reduced brood size due to defective pachytene exit from meiosis I. gla-3 encodes a TIS11-like zinc-finger-containing protein that is expressed in the germline, from the L4 larval stage to adulthood. Germ stem cells are the precursors to all subsequent generations in a species, and, therefore, germ cell formation is tightly monitored to ensure high-fidelity transfer of the genetic material. Germ cell genome integrity is monitored at several checkpoints, allowing for DNA repair, cell cycle arrest, and apoptosis when required. In mammals, inactivation of genes with checkpoint function frequently results in aberrant cell death and infertility (Lim and Hasty 1996;Bender et al. 2002). Germ cell development is also characterized by either massive waves or low but constant levels of apoptosis that are not caused by genetic defects. For example, >99.9% of oocytes undergo apoptosis in response to hormonal changes that occur at several stages during the female life cycle in mammals (Tilly 2001;Kim and Tilly 2004). Apoptosis is also the fate of ∼50% of germ cells undergoing oogenesis in the gonad of Caenorhabditis elegans hermaphrodites. (Gumienny et al. 1999). Characterization of the pathways that regulate germ cell death will contribute to our understanding of the cell suicide decision and might allow for more efficient therapeutic manipulation of the apoptotic program.C. elegans is a good model to study the signaling cascades involved in the decision between germ cell survival and germ cell death (Hengartner 1997;Gumienny et al. 1999). The adult hermaphrodite gonads consist of two U-shaped tubes that are connected at a common uterus. At the distal end of each gonad, mitotic germ stem cells proliferate in response to the Notch ligand LAG-2. Cells beyond the influence of LAG-2 enter meiosis and progress through the pachytene stage of meiosis I; this transition requires activation of the RAS/MAPK (MAP kinase) signaling cascade (Hubbard and Greenstein 2000;Seydoux and Schedl 2001). Following transition through pachytene, germ cells can either enter diakinesis of meiosis I and differentiate into oocytes or undergo apoptosis. We previously suggested that these cell deaths are the result of a physiological, homeostatic control mechanism that limits the number of germ cells permitted to differentiate into oocytes (Gumienny et al. 1999).

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Section: Identification Of Mutations In the C Elegans Gla-3 Genementioning

confidence: 99%

C. elegans GLA-3 is a novel component of the MAP kinase MPK-1 signaling pathway required for germ cell survival

Kritikou

Milstein²,

Vidalain³

et al. 2006

Genes Dev.

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“…These effects have suggested that establishment of anterior and posterior PAR domains depends on antagonistic interactions between the PAR-3/PAR-6/PKC-3 complex in the anterior and PAR-2 in the posterior. In contrast, mutations in par-1, mex-5 and mex-6 were reported not to affect PAR localization in the zygote (Etemad-Moghadam et al, 1995;Boyd et al, 1996;Tabuse et al, 1998;Hung and Kemphues, 1999;Schubert et al, 2000). These mutations, however, have a dramatic effect on the distribution of several cell fate regulators.…”

Section: Introductionmentioning

confidence: 99%

“…PAR-1 in turn is required for asymmetric spindle positioning and for the asymmetric localization of several developmental regulators . PAR-1 exerts its influence on developmental regulators through MEX-5 and MEX-6, two redundant cytoplasmic CCCH finger proteins (Schubert et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Polarization of theC. eleganszygote proceeds via distinct establishment and maintenance phases

et al. 2003

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Polarization of the C. elegans zygote along the anteriorposterior axis depends on cortically enriched (PAR) and cytoplasmic (MEX-5/6) proteins, which function together to localize determinants (e.g. PIE-1) in response to a polarizing cue associated with the sperm asters. Using timelapse microscopy and GFP fusions, we have analyzed the localization dynamics of PAR-2, PAR-6, MEX-5, MEX-6 and PIE-1 in wild-type and mutant embryos. These studies reveal that polarization involves two genetically and temporally distinct phases.

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“…In rare cases where nucleotide sequence is highly conserved, RNAi with a single trigger molecule can target multiple family members (e.g., Colombo et al, 2003). If the number of family members is small, it is possible to reveal redundancies by double or triple knockout or knockdown (e.g., Schubert et al, 2000; Gotta and Ahringer, Essential genes 2001). Redundant pathways, in which different processes can accomplish the same essential function, are more cryptic and are not likely to be detected except by fortuitous double mutant combinations or screens for synthetic lethal mutations (enhancers).…”

Section: Redundancy Of Essential Genesmentioning

confidence: 99%

Essential genes

Kemphues¹

2005

WormBook

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MEX-5 and MEX-6 Function to Establish Soma/Germline Asymmetry in Early C. elegans Embryos

Cited by 234 publications

References 48 publications

C. elegans GLA-3 is a novel component of the MAP kinase MPK-1 signaling pathway required for germ cell survival

C. elegans GLA-3 is a novel component of the MAP kinase MPK-1 signaling pathway required for germ cell survival

Polarization of theC. eleganszygote proceeds via distinct establishment and maintenance phases

Essential genes

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