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Centriole Duplication, Neural Stem Cell Division, and Tumorigenesis
Centrioles are essential components of the centrosomes, which are required for the formation of the mitotic spindles, cilia, and flagella. Centriole duplication involves the growth of a procentriole (daughter centriole) from an existing centriole (mother centriole). Primary microcephaly (MCPH) is characterized by a substantial reduction in size of the cerebral cortex with mild to severe mental retardation. Recently, mutations in many centriolar genes were reported to cause MCPH and ciliopathies, but their underlining mechanisms remain unclear. During the past years, our lab has identified several key proteins that participate in centriole duplication and cilia formation. We found that CPAP cooperates with CEP120 to regulate centriole length (Nat Cell Biol. 2009; J Cell Biol 2013; Sci Rep 2019). We further demonstrated that CPAP could interact and form separate complexes with STIL (EMBO J, 2011), CEP135 (EMBO J, 2013), and CEP120 (J Cell Biol, 2013), and such interaction complexes as well as the RTTN-STIL interactions (Nat Commun, 2017) are critical to build a full-length centriole. In addition, we also found that Myosin-Va mediates the initial transportation of preciliary vesicles to the mother centriole, that defines the onset of ciliogenesis. (Nat Cell Biol 2018). Recent reports showed that uncontrolled centriole/centrosome replication might lead to unrestrained proliferation and cause chromosome instability in cancers. In the future, we will use a combination of cellular, molecular, genetic, animal model, and hiPS-derived organoid approaches to understand how the cellular organelles (centrioles or cilia) are established and how mutations in centriolar genes cause primary microcephaly, ciliopathies, and tumorigenesis in humans.
Centriole Duplication, Neural Stem Cell Division, and Tumorigenesis
Centrioles are essential components of the centrosomes, which are required for the formation of the mitotic spindles, cilia, and flagella. Centriole duplication involves the growth of a procentriole (daughter centriole) from an existing centriole (mother centriole). Primary microcephaly (MCPH) is characterized by a substantial reduction in size of the cerebral cortex with mild to severe mental retardation. Recently, mutations in many centriolar genes were reported to cause MCPH and ciliopathies, but their underlining mechanisms remain unclear. During the past years, our lab has identified several key proteins that participate in centriole duplication and cilia formation. We found that CPAP cooperates with CEP120 to regulate centriole length (Nat Cell Biol. 2009; J Cell Biol 2013; Sci Rep 2019). We further demonstrated that CPAP could interact and form separate complexes with STIL (EMBO J, 2011), CEP135 (EMBO J, 2013), and CEP120 (J Cell Biol, 2013), and such interaction complexes as well as the RTTN-STIL interactions (Nat Commun, 2017) are critical to build a full-length centriole. In addition, we also found that Myosin-Va mediates the initial transportation of preciliary vesicles to the mother centriole, that defines the onset of ciliogenesis. (Nat Cell Biol 2018). Recent reports showed that uncontrolled centriole/centrosome replication might lead to unrestrained proliferation and cause chromosome instability in cancers. In the future, we will use a combination of cellular, molecular, genetic, animal model, and hiPS-derived organoid approaches to understand how the cellular organelles (centrioles or cilia) are established and how mutations in centriolar genes cause primary microcephaly, ciliopathies, and tumorigenesis in humans.
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Justine Guguin, Ting-Yu Chen,Alicia Besson,Silvestre Cuinat,Eloise Bertiaux,Lucile Boutaud, Nolan Ardito, Miren Imaz Murguiondo, Sarah Cabet,Virginie Hamel,Sophie Thomas,Bertrand Pain,
medrxiv(2024)
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