Analysis of centriole elimination during<i>C. elegans</i>oogenesis

Mikeladze-Dvali, Tamara; Tobel, Lukas von; Strnad, Petr; Knott, Graham; Heinrich, Leonhardt; Schermelleh, Lothar; Gönczy, Pierre

doi:10.1242/dev.075440

Cited by 61 publications

(75 citation statements)

References 82 publications

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“…This CE mechanism has also been observed in worms (Mikeladze-Dvali et al, 2012), suggesting an ancient origin for CE maintained throughout evolution. More work will be required, but the footing has suddenly become more solid for future excursions into CE.…”

supporting

confidence: 58%

“…Alternatively, CD might involve MT depolymerization machinery that specifically attacks the centriole barrel, effectively reversing the normal centriole elongation machinery that occurs during centriole duplication. Novel proteins could also contribute to CD; the helicase CGH-1, for example, somehow delays CE in worms (Mikeladze-Dvali et al, 2012). Do other unsuspected mechanisms exist?…”

mentioning

confidence: 99%

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Taking Centrioles to the Elimination Round

Schoborg

Rusan

2016

Developmental Cell

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supporting

confidence: 58%

mentioning

confidence: 99%

Taking Centrioles to the Elimination Round

Schoborg

Rusan

2016

Developmental Cell

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“…In this case, acentriolar MTOCs coordinate asymmetric cell divisions producing oocyte polar bodies. [18][19][20] To our knowledge, the presence of CDK1 on meiotic centrosomes has not been directly demonstrated. Nonetheless, protein kinase B, implicated in the initial activation of CDK1 in mouse oocytes, has been found to localize to acentriolar meiotic centrosomes.…”

Section: Introductionmentioning

confidence: 99%

Functional specialization of chordate CDK1 paralogs during oogenic meiosis

et al. 2015

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Cyclin-dependent kinases (CDKs) are central regulators of eukaryotic cell cycle progression. In contrast to interphase CDKs, the mitotic phase CDK1 is the only CDK capable of driving the entire cell cycle and it can do so from yeast to mammals. Interestingly, plants and the marine chordate, Oikopleura dioica, possess paralogs of the highly conserved CDK1 regulator. However, whereas in plants the 2 CDK1 paralogs replace interphase CDK functions, O. dioica has a full complement of interphase CDKs in addition to its 5 odCDK1 paralogs. Here we show specific sub-functionalization of odCDK1 paralogs during oogenesis. Differential spatiotemporal dynamics of the odCDK1a, d and e paralogs and the meiotic polo-like kinase 1 (Plk1) and aurora kinase determine the subset of meiotic nuclei in prophase I arrest that will seed growing oocytes and complete meiosis. Whereas we find odCDK1e to be non-essential, knockdown of the odCDK1a paralog resulted in the spawning of non-viable oocytes of reduced size. Knockdown of odCDK1d also resulted in the spawning of non-viable oocytes. In this case, the oocytes were of normal size, but were unable to extrude polar bodies upon exposure to sperm, because they were unable to resume meiosis from prophase I arrest, a classical function of the sole CDK1 during meiosis in other organisms. Thus, we reveal specific sub-functionalization of CDK1 paralogs, during the meiotic oogenic program.

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“…Instead, they abort anaphase I, skip meiosis II entirely, and enter mitosis. The mitotic cells exhibit signs of cell-cycle progression, such as nuclear envelope breakdown and reformation, but they do not divide, possibly because they lack the centrioles normally contributed by the sperm (Albertson 1984;Mikeladze-Dvali et al 2012). These results suggest that, upon fertilization, sperm normally contribute a second signal that stimulates the egg to extrude the first polar body and initiate meiosis II.…”

mentioning

confidence: 92%

Maternal MEMI Promotes Female Meiosis II in Response to Fertilization in Caenorhabditis elegans

Ataeian

Tegha-Dunghu

Curtis³

et al. 2016

Genetics

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In most animals, female meiosis completes only after fertilization. Sperm entry has been implicated in providing a signal for the initiation of the final meiotic processes; however, a maternal component required for this process has not been previously identified. We report the characterization of a novel family of three highly similar paralogs (memi-1, memi-2, memi-3) that encode oocyte-specific proteins. A hyper-morphic mutation memi-1(sb41) results in failure to exit female meiosis II properly; however, loss of all three paralogs results in a "skipped meiosis II" phenotype. Mutations that prevent fertilization, such as fer-1(hc1), also cause a skipped meiosis II phenotype, suggesting that the MEMI proteins represent a maternal component of a postfertilization signal that specifies the meiosis II program. MEMI proteins are degraded before mitosis and sensitive to ZYG-11, a substrate-specific adapter for cullin-based ubiquitin ligase activity, and the memi-1(sb41) mutation results in inappropriate persistence of the MEMI-1 protein into mitosis. Using an RNAi screen for suppressors of memi-1(sb41), we identified a sperm-specific PP1 phosphatase, GSP-3/4, as a putative sperm component of the MEMI pathway. We also found that MEMI and GSP-3/4 proteins can physically interact via co-immunoprecipitation. These results suggest that sperm-specific PP1 and maternal MEMI proteins act in the same pathway after fertilization to facilitate proper meiosis II and the transition into embryonic mitosis.

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Analysis of centriole elimination duringC. elegansoogenesis

Cited by 61 publications

References 82 publications

Taking Centrioles to the Elimination Round

Taking Centrioles to the Elimination Round

Functional specialization of chordate CDK1 paralogs during oogenic meiosis

Maternal MEMI Promotes Female Meiosis II in Response to Fertilization in Caenorhabditis elegans

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