The role of sumoylation in senescence

Lyndee L. Scurr, Sebastian Haferkamp, Helen Rizos*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Cellular senescence is a program initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions and telomere attrition. Once engaged senescence irreversibly limits cellular proliferation and potently prevents tumor formation in vivo. The precise mechanisms driving the onset of senescence are still not completely defined, although the pRb and p53 tumor suppressor pathways converge with the SUMO cascade to regulate cellular senescence. Sumoylation translocates p53 to PML nuclear bodies where it can co-operate with many sumoylated co-factors in a program that activates pRb and favors senescence. Once activated pRb integrates various proteins, many of them sumoylated, into a repressor complex that inhibits the transcription of proliferation-promoting genes and initiates chromatin condensation. Sumoylation is required for heterochromatin formation during senescence and may act as a scaffold to stabilize the pRb repressor complex. Thus, SUMO is a critical component of a tumor-suppressor network that limits aberrant cell proliferation and tumorigenesis.

Original languageEnglish
Title of host publicationSUMO Regulation of Cellular Processes
EditorsVan G. Wilson
Place of PublicationDordrecht
PublisherSpringer, Springer Nature
Pages201-216
Number of pages16
ISBN (Electronic)9789048126491
ISBN (Print)9789048126484
DOIs
Publication statusPublished - 2009
Externally publishedYes

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