The γ-tubulin meshwork assists in the recruitment of PCNA to chromatin in mammalian cells
(2021) In Communications Biology 4.- Abstract
- Changes in the location of γ-tubulin ensure cell survival and preserve genome integrity. We investigated whether the nuclear accumulation of γ-tubulin facilitates the transport of proliferating cell nuclear antigen (PCNA) between the cytosolic and the nuclear compartment in mammalian cells. We found that the γ-tubulin meshwork assists in the recruitment of PCNA to chromatin. Also, decreased levels of γ-tubulin reduce the nuclear pool of PCNA. In addition, the γ-tubulin C terminus encodes a PCNA-interacting peptide (PIP) motif, and a γ-tubulin–PIP-mutant affects the nuclear accumulation of PCNA. In a cell-free system, PCNA and γ-tubulin formed a complex. In tumors, there is a significant positive correlation between TUBG1 and PCNA... (More)
- Changes in the location of γ-tubulin ensure cell survival and preserve genome integrity. We investigated whether the nuclear accumulation of γ-tubulin facilitates the transport of proliferating cell nuclear antigen (PCNA) between the cytosolic and the nuclear compartment in mammalian cells. We found that the γ-tubulin meshwork assists in the recruitment of PCNA to chromatin. Also, decreased levels of γ-tubulin reduce the nuclear pool of PCNA. In addition, the γ-tubulin C terminus encodes a PCNA-interacting peptide (PIP) motif, and a γ-tubulin–PIP-mutant affects the nuclear accumulation of PCNA. In a cell-free system, PCNA and γ-tubulin formed a complex. In tumors, there is a significant positive correlation between TUBG1 and PCNA expression. Thus, we report a novel mechanism that constitutes the basis for tumor growth by which the γ-tubulin meshwork maintains indefinite proliferation by acting as an opportune scaffold for the transport of PCNA from the cytosol to the chromatin. (Less)
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https://lup.lub.lu.se/record/649b91bd-75c4-4521-94b0-c61baa2ca149
- author
- organization
- publishing date
- 2021-06-22
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Communications Biology
- volume
- 4
- article number
- 767
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:85108581941
- pmid:34158617
- ISSN
- 2399-3642
- DOI
- 10.1038/s42003-021-02280-1
- language
- English
- LU publication?
- yes
- id
- 649b91bd-75c4-4521-94b0-c61baa2ca149
- date added to LUP
- 2021-06-22 11:40:09
- date last changed
- 2024-02-20 08:37:06
@article{649b91bd-75c4-4521-94b0-c61baa2ca149, abstract = {{Changes in the location of γ-tubulin ensure cell survival and preserve genome integrity. We investigated whether the nuclear accumulation of γ-tubulin facilitates the transport of proliferating cell nuclear antigen (PCNA) between the cytosolic and the nuclear compartment in mammalian cells. We found that the γ-tubulin meshwork assists in the recruitment of PCNA to chromatin. Also, decreased levels of γ-tubulin reduce the nuclear pool of PCNA. In addition, the γ-tubulin C terminus encodes a PCNA-interacting peptide (PIP) motif, and a γ-tubulin–PIP-mutant affects the nuclear accumulation of PCNA. In a cell-free system, PCNA and γ-tubulin formed a complex. In tumors, there is a significant positive correlation between TUBG1 and PCNA expression. Thus, we report a novel mechanism that constitutes the basis for tumor growth by which the γ-tubulin meshwork maintains indefinite proliferation by acting as an opportune scaffold for the transport of PCNA from the cytosol to the chromatin.}}, author = {{Corvaisier, Matthieu and Zhou, Jingkai and Malycheva, Darina and Cornella, Nicola and Chioureas, Dimitrios and Gustafsson, Nina and Rosselló, Catalina Ana and Ayora, Silvia and Li, Tongbin and Ekström-Holka, Kristina and Jirström, Karin and Lindström, Lisa and Alvarado Kristensson, Maria}}, issn = {{2399-3642}}, language = {{eng}}, month = {{06}}, publisher = {{Nature Publishing Group}}, series = {{Communications Biology}}, title = {{The γ-tubulin meshwork assists in the recruitment of PCNA to chromatin in mammalian cells}}, url = {{http://dx.doi.org/10.1038/s42003-021-02280-1}}, doi = {{10.1038/s42003-021-02280-1}}, volume = {{4}}, year = {{2021}}, }