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CEP215_gallus_interactome - A CEP215-HSET complex links centrosomes with spindle poles and drives centrosome clustering in cancer

ABSTRACT: To establish the molecular basis for CEP215 function in centrosome-spindle pole attachment, we employed an unbiased proteomic approach to isolat e and identify CEP215 interactors. To this end, affinity purification tags ( Gs TAP containing protein G and streptavidin-binding protein) were inserted in-frame into both alleles of the CEP215 gene (CEP215-TAP cell line) in the chicken B cell line, DT40. Following affinity purification, protein complexes were analysed by mass spectr ometry

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Gallus Gallus (chicken)

TISSUE(S): B Cell

SUBMITTER: Pavithra Lakshminarasimhan

LAB HEAD: Fanni gergely

PROVIDER: PXD003382 | Pride | 2016-03-31

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	AP_TAPFL_1.msf	Msf
	AP_TAPFL_1.raw	Raw
	AP_TAPFL_2.msf	Msf
	AP_TAPFL_2.raw	Raw
	AP_TAPFL_3-01.msf	Msf

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Publications

A CEP215-HSET complex links centrosomes with spindle poles and drives centrosome clustering in cancer.

Chavali Pavithra L PL Chandrasekaran Gayathri G Barr Alexis R AR Tátrai Péter P Taylor Chris C Papachristou Evaggelia K EK Woods C Geoffrey CG Chavali Sreenivas S Gergely Fanni F

Nature communications 20160318

Numerical centrosome aberrations underlie certain developmental abnormalities and may promote cancer. A cell maintains normal centrosome numbers by coupling centrosome duplication with segregation, which is achieved through sustained association of each centrosome with a mitotic spindle pole. Although the microcephaly- and primordial dwarfism-linked centrosomal protein CEP215 has been implicated in this process, the molecular mechanism responsible remains unclear. Here, using proteomic profiling ...[more]

PMID: 26987684

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A CEP215-HSET complex links centrosomes with spindle poles and drives centrosome clustering in cancer.

Project description:Numerical centrosome aberrations underlie certain developmental abnormalities and may promote cancer. A cell maintains normal centrosome numbers by coupling centrosome duplication with segregation, which is achieved through sustained association of each centrosome with a mitotic spindle pole. Although the microcephaly- and primordial dwarfism-linked centrosomal protein CEP215 has been implicated in this process, the molecular mechanism responsible remains unclear. Here, using proteomic profiling, we identify the minus end-directed microtubule motor protein HSET as a direct binding partner of CEP215. Targeted deletion of the HSET-binding domain of CEP215 in vertebrate cells causes centrosome detachment and results in HSET depletion at centrosomes, a phenotype also observed in CEP215-deficient patient-derived cells. Moreover, in cancer cells with centrosome amplification, the CEP215-HSET complex promotes the clustering of extra centrosomes into pseudo-bipolar spindles, thereby ensuring viable cell division. Therefore, stabilization of the centrosome-spindle pole interface by the CEP215-HSET complex could promote survival of cancer cells containing supernumerary centrosomes.

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