Abstract:
:DDB1, a component of the Cul4 ubiquitin ligase complex, promotes protein ubiquitination in diverse cellular functions, including nuclear excision repair, regulation of the cell cycle, and DNA replication. To investigate its physiological significance, we generated mice with null and floxed alleles of the DDB1 gene. Here we report that null mutation of DDB1 caused early embryonic lethality, while conditional inactivation of the gene in brain and lens led to neuronal and lens degeneration, brain hemorrhages, and neonatal death. These defects stemmed from a selective elimination of nearly all proliferating neuronal progenitor cells and lens epithelial cells by apoptosis. The cell death was preceded by aberrant accumulation of cell cycle regulators and increased genomic instability and could be partially rescued by removal of the tumor suppressor protein p53. Our results indicate that DDB1 plays an essential role in maintaining viability and genomic integrity of dividing cells.
journal_name
Celljournal_title
Cellauthors
Cang Y,Zhang J,Nicholas SA,Bastien J,Li B,Zhou P,Goff SPdoi
10.1016/j.cell.2006.09.045subject
Has Abstractpub_date
2006-12-01 00:00:00pages
929-40issue
5eissn
0092-8674issn
1097-4172pii
S0092-8674(06)01406-1journal_volume
127pub_type
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