Role of a novel coiled-coil domain-containing protein CCDC69 in regulating central spindle assembly

Pal, Debjani; Wu, Di; Haruta, Akiko; Matsumura, Fumio; Wei, Qize

doi:10.4161/cc.9.20.13387

Cited by 20 publications

(22 citation statements)

References 67 publications

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“…This down‐regulation may increase oxidative stress within the oocyte. Spindle defects may also be aggravated by repression of Pak4 and Ccdc69 (Table ), two proteins known to affect spindle assembly (Pal et al , ; Bompard et al , ). RT–qPCR experiments confirmed the down‐regulation of Ccdc69 and Eef1e1 in GV oocytes ().…”

Section: Resultsmentioning

confidence: 99%

PATL 2 is a key actor of oocyte maturation whose invalidation causes infertility in women and mice

et al. 2018

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The genetic causes of oocyte meiotic deficiency (OMD), a form of primary infertility characterised by the production of immature oocytes, remain largely unexplored. Using whole exome sequencing, we found that 26% of a cohort of 23 subjects with OMD harboured the same homozygous nonsense pathogenic mutation in PATL2, a gene encoding a putative RNA‐binding protein. Using Patl2 knockout mice, we confirmed that PATL2 deficiency disturbs oocyte maturation, since oocytes and zygotes exhibit morphological and developmental defects, respectively. PATL2's amphibian orthologue is involved in the regulation of oocyte mRNA as a partner of CPEB. However, Patl2's expression profile throughout oocyte development in mice, alongside colocalisation experiments with Cpeb1, Msy2 and Ddx6 (three oocyte RNA regulators) suggest an original role for Patl2 in mammals. Accordingly, transcriptomic analysis of oocytes from WT and Patl2 −/− animals demonstrated that in the absence of Patl2, expression levels of a select number of highly relevant genes involved in oocyte maturation and early embryonic development are deregulated. In conclusion, PATL2 is a novel actor of mammalian oocyte maturation whose invalidation causes OMD in humans.

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Section: Resultsmentioning

confidence: 99%

PATL 2 is a key actor of oocyte maturation whose invalidation causes infertility in women and mice

et al. 2018

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“…In addition to cytokines, genes that regulate gene expression are differentially expressed in progenitors for distinct adipocyte subtypes. For example, progenitors of Cluster 1, which represents adipocytes with high lipogenic capacity, are highly enriched in CCDC69, a coiled-coil domain protein implicated in central spindle assembly [52], which is enriched in human adipose tissue (www.proteinatlas.org/ENSG00000198624-CCDC69/tissue). The 21 genes decreased in Cluster 2 relative to other clones mapped significantly to MAD box and basic helix-loop-helix gene families (MEF2C, ID1 and NPAS1).…”

Section: Discussionmentioning

confidence: 99%

“Multiple human adipocyte subtypes and mechanisms of their development”

Desai

Yang

et al. 2019

Preprint

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Human adipose tissue depots perform numerous diverse physiological functions, and are differentially linked to metabolic disease risk, yet only two major human adipocyte subtypes have been described, white and "brown/brite/beige." The diversity and lineages of adipocyte classes have been studied in mice using genetic methods that cannot be applied in humans. Here we circumvent this problem by studying the fate of single mesenchymal progenitor cells obtained from human adipose tissue. We report that a minimum of four human adipocyte subtypes can be distinguished by transcriptomic analysis, specialized for functionally distinct processes such as adipokine secretion and thermogenesis. Evidence for the presence of these adipocytes subtypes in adult humans is evidenced by differential expression of key adipokines leptin and adiponectin in isolated mature adipocytes. The human adipocytes most similar to the mouse "brite/beige" adipocytes are enriched in mechanisms that promote iron accumulation and protect from oxidative stress, and are derived from progenitors that express high levels of cytokines such as IL1B, IL8, IL11 and the IL6 family cytokine LIF, and low levels of the transcriptional repressors ID1 and ID3. Our finding of this adipocyte repertoire and its developmental mechanisms provides a high-resolution framework to analyze human adipose tissue architecture and its role in systemic metabolism and metabolic disease.

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“…Coimmunoprecipitation Assays-Coimmunoprecipitation assays were carried out as described previously (46,47). Briefly, transfected HeLa cells were lysed in radioimmune precipitation lysis buffer (50 mM Tris-HCl (pH 7.4), 150 mM NaCl, 1% Nonidet P-40, 2.5% sodium deoxycholate, 1 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, 1 g/ml aprotinin, 1 g/ml leupeptin, 1 g/ml pepstatin, 1 mM Na 3 VO 4 , 1 mM NaF) for 10 min on ice.…”

Section: Methodsmentioning

confidence: 99%

Phosphorylation of Myosin II-interacting Guanine Nucleotide Exchange Factor (MyoGEF) at Threonine 544 by Aurora B Kinase Promotes the Binding of Polo-like Kinase 1 to MyoGEF

Asiedu

Matsumura

et al. 2014

Journal of Biological Chemistry

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Background: Aurora B kinase (aurora B) and polo-like kinase 1 (Plk1) are critical regulators of cytokinesis. Results: Phosphorylation of MyoGEF at Thr-544 by aurora B promotes the binding of Plk1 to MyoGEF. Conclusion: Phosphorylation of MyoGEF by aurora B creates a docking site for Plk1. Significance: Coordinated regulation of MyoGEF localization and activation by aurora B and Plk1 contributes to the regulation of cytokinesis.

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Role of a novel coiled-coil domain-containing protein CCDC69 in regulating central spindle assembly

Cited by 20 publications

References 67 publications

PATL 2 is a key actor of oocyte maturation whose invalidation causes infertility in women and mice

PATL 2 is a key actor of oocyte maturation whose invalidation causes infertility in women and mice

“Multiple human adipocyte subtypes and mechanisms of their development”

Phosphorylation of Myosin II-interacting Guanine Nucleotide Exchange Factor (MyoGEF) at Threonine 544 by Aurora B Kinase Promotes the Binding of Polo-like Kinase 1 to MyoGEF

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