Deuterosome-Mediated Centriole Biogenesis

Deborah A. KlosDehring; Eszter K. Vladar; Michael E. Werner; Jennifer W. Mitchell; Peter Hwang; Brian J. Mitchell

doi:10.1016/j.devcel.2013.08.021

Deuterosome-Mediated Centriole Biogenesis

Deborah A. KlosDehring, Eszter K. Vladar, Michael E. Werner, Jennifer W. Mitchell, Peter Hwang, Brian J. Mitchell^*

^*Corresponding author for this work

Cell & Developmental Biology

Research output: Contribution to journal › Article › peer-review

118 Scopus citations

Abstract

The ability of cells to faithfully duplicate their two centrioles once per cell cycle is critical for proper mitotic progression and chromosome segregation. Multiciliated cells represent an interesting variation of centriole duplication in that these cells generate greater than 100 centrioles, which form the basal bodies of their motile cilia. This centriole amplification is proposed to require a structure termed the deuterosome, thought to be capable of promoting de novo centriole biogenesis. Here, we begin to molecularly characterize the deuterosome and identify it as a site for the localization of Cep152, Plk4, andSAS6. Additionally we identify CCDC78 as a centriole-associated and deuterosome protein that is essential for centriole amplification. Overexpression of Cep152, but not Plk4, SAS6, or CCDC78, drives overamplification of centrioles. However, in CCDC78 morphants, Cep152 fails to localize to the deuterosome and centriole biogenesis is impaired, indicating that CCDC78-mediated recruitment of Cep152 is required for deuterosome-mediated centriole biogenesis.

Original language	English (US)
Pages (from-to)	103-112
Number of pages	10
Journal	Developmental Cell
Volume	27
Issue number	1
DOIs	https://doi.org/10.1016/j.devcel.2013.08.021
State	Published - Oct 14 2013

Funding

This work was supported by the NIH/NIGMS (R01GM089970 to B.J.M.) and by a pilot grant from the NU-SDRC NIH/NIAMS (5P30AR057216-05). D.A.K.D. was supported by an ARRA NRSA grant (1F32AI08006901A1), and M.E.W. was supported by a postdoctoral fellowship from the American Heart Association.

ASJC Scopus subject areas

Molecular Biology
General Biochemistry, Genetics and Molecular Biology
Developmental Biology
Cell Biology

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10.1016/j.devcel.2013.08.021

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title = "Deuterosome-Mediated Centriole Biogenesis",

abstract = "The ability of cells to faithfully duplicate their two centrioles once per cell cycle is critical for proper mitotic progression and chromosome segregation. Multiciliated cells represent an interesting variation of centriole duplication in that these cells generate greater than 100 centrioles, which form the basal bodies of their motile cilia. This centriole amplification is proposed to require a structure termed the deuterosome, thought to be capable of promoting de novo centriole biogenesis. Here, we begin to molecularly characterize the deuterosome and identify it as a site for the localization of Cep152, Plk4, andSAS6. Additionally we identify CCDC78 as a centriole-associated and deuterosome protein that is essential for centriole amplification. Overexpression of Cep152, but not Plk4, SAS6, or CCDC78, drives overamplification of centrioles. However, in CCDC78 morphants, Cep152 fails to localize to the deuterosome and centriole biogenesis is impaired, indicating that CCDC78-mediated recruitment of Cep152 is required for deuterosome-mediated centriole biogenesis.",

author = "KlosDehring, \{Deborah A.\} and Vladar, \{Eszter K.\} and Werner, \{Michael E.\} and Mitchell, \{Jennifer W.\} and Peter Hwang and Mitchell, \{Brian J.\}",

note = "Funding Information: This work was supported by the NIH/NIGMS (R01GM089970 to B.J.M.) and by a pilot grant from the NU-SDRC NIH/NIAMS (5P30AR057216-05). D.A.K.D. was supported by an ARRA NRSA grant (1F32AI08006901A1), and M.E.W. was supported by a postdoctoral fellowship from the American Heart Association. ",

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AU - Vladar, Eszter K.

AU - Werner, Michael E.

AU - Mitchell, Jennifer W.

AU - Hwang, Peter

AU - Mitchell, Brian J.

N1 - Funding Information: This work was supported by the NIH/NIGMS (R01GM089970 to B.J.M.) and by a pilot grant from the NU-SDRC NIH/NIAMS (5P30AR057216-05). D.A.K.D. was supported by an ARRA NRSA grant (1F32AI08006901A1), and M.E.W. was supported by a postdoctoral fellowship from the American Heart Association.

PY - 2013/10/14

Y1 - 2013/10/14

N2 - The ability of cells to faithfully duplicate their two centrioles once per cell cycle is critical for proper mitotic progression and chromosome segregation. Multiciliated cells represent an interesting variation of centriole duplication in that these cells generate greater than 100 centrioles, which form the basal bodies of their motile cilia. This centriole amplification is proposed to require a structure termed the deuterosome, thought to be capable of promoting de novo centriole biogenesis. Here, we begin to molecularly characterize the deuterosome and identify it as a site for the localization of Cep152, Plk4, andSAS6. Additionally we identify CCDC78 as a centriole-associated and deuterosome protein that is essential for centriole amplification. Overexpression of Cep152, but not Plk4, SAS6, or CCDC78, drives overamplification of centrioles. However, in CCDC78 morphants, Cep152 fails to localize to the deuterosome and centriole biogenesis is impaired, indicating that CCDC78-mediated recruitment of Cep152 is required for deuterosome-mediated centriole biogenesis.

AB - The ability of cells to faithfully duplicate their two centrioles once per cell cycle is critical for proper mitotic progression and chromosome segregation. Multiciliated cells represent an interesting variation of centriole duplication in that these cells generate greater than 100 centrioles, which form the basal bodies of their motile cilia. This centriole amplification is proposed to require a structure termed the deuterosome, thought to be capable of promoting de novo centriole biogenesis. Here, we begin to molecularly characterize the deuterosome and identify it as a site for the localization of Cep152, Plk4, andSAS6. Additionally we identify CCDC78 as a centriole-associated and deuterosome protein that is essential for centriole amplification. Overexpression of Cep152, but not Plk4, SAS6, or CCDC78, drives overamplification of centrioles. However, in CCDC78 morphants, Cep152 fails to localize to the deuterosome and centriole biogenesis is impaired, indicating that CCDC78-mediated recruitment of Cep152 is required for deuterosome-mediated centriole biogenesis.

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Deuterosome-Mediated Centriole Biogenesis

Abstract

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