The Saccharomyces cerevisiae Rad53 protein kinase is required for the execution of checkpoint arrest at multiple stages of the cell cycle, We found that Rad53 autophosphorylation activity depends on in trails phosphorylation mediated by Mec1 and does not require physical association with other proteins. Uncoupling in trans phosphorylation from autophosphorylation using a rad53 kinase-defective mutant results in a dominant-negative checkpoint defect. Activation of Rad53 in response to DNA damage in G(1) requires the Rad9, Mec3, Ddc1, Rad17 and Rad24 checkpoint factors, while this dependence is greatly reduced in S phase cells. Furthermore, during recovery from checkpoint activation, Rad53 activity decreases through a process that does not require protein synthesis, We also found that Rad53 modulates the lagging strand replication apparatus by controlling phosphorylation of the DNA polymerase a-primase complex in response to intra-S DNA damage.

Activation of Rad53 kinase in response to DNA damage and its effect in modulating phosphorylation of the lagging strand DNA polymerase / A. Pellicioli, C. Lucca, G. Liberi, F. Marini, M. Lopes, P. Plevani, A. Romano, P.P. Di Fiore, M. Foiani. - In: EMBO JOURNAL. - ISSN 0261-4189. - 18:22(1999 Nov 15), pp. 6561-6572.

Activation of Rad53 kinase in response to DNA damage and its effect in modulating phosphorylation of the lagging strand DNA polymerase

A. Pellicioli
Primo
;
G. Liberi;F. Marini;P. Plevani;P.P. Di Fiore
Penultimo
;
M. Foiani
Ultimo
1999

Abstract

The Saccharomyces cerevisiae Rad53 protein kinase is required for the execution of checkpoint arrest at multiple stages of the cell cycle, We found that Rad53 autophosphorylation activity depends on in trails phosphorylation mediated by Mec1 and does not require physical association with other proteins. Uncoupling in trans phosphorylation from autophosphorylation using a rad53 kinase-defective mutant results in a dominant-negative checkpoint defect. Activation of Rad53 in response to DNA damage in G(1) requires the Rad9, Mec3, Ddc1, Rad17 and Rad24 checkpoint factors, while this dependence is greatly reduced in S phase cells. Furthermore, during recovery from checkpoint activation, Rad53 activity decreases through a process that does not require protein synthesis, We also found that Rad53 modulates the lagging strand replication apparatus by controlling phosphorylation of the DNA polymerase a-primase complex in response to intra-S DNA damage.
No
English
Checkpoints; DNA damage; DNA polymerase α-primase; DNA replication; Rad53
Settore BIO/11 - Biologia Molecolare
Articolo
Esperti anonimi
Pubblicazione scientifica
15-nov-1999
Oxford University Press
18
22
6561
6572
12
Pubblicato
Periodico con rilevanza internazionale
Pubmed
info:eu-repo/semantics/article
Activation of Rad53 kinase in response to DNA damage and its effect in modulating phosphorylation of the lagging strand DNA polymerase / A. Pellicioli, C. Lucca, G. Liberi, F. Marini, M. Lopes, P. Plevani, A. Romano, P.P. Di Fiore, M. Foiani. - In: EMBO JOURNAL. - ISSN 0261-4189. - 18:22(1999 Nov 15), pp. 6561-6572.
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262
Article (author)
si
A. Pellicioli, C. Lucca, G. Liberi, F. Marini, M. Lopes, P. Plevani, A. Romano, P.P. Di Fiore, M. Foiani
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/154840
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