Reference Report

Reference
Citation	Xu, J., Xin, S., Du, W. (2001). Drosophila Chk2 is required for DNA damage-mediated cell cycle arrest and apoptosis. FEBS Lett. 508(3): 394--398. (Export to RIS)
FlyBase ID	FBrf0141530
Publication Type	Research paper
PubMed ID	11728459
PubMed Abstract	Chk2 is a major target of ataxia telangiectasia-mutated (ATM) and ATM- and Rad3-related (ATR). Germline mutations in Chk2 have been identified in a subset of patients with Li-Fraumeni syndrome, suggesting that Chk2 is a tumor suppressor gene. To investigate the role of Chk2 in multicellular organisms, a Drosophila chk2 (Dmchk2) mutant was generated. Dmchk2 mutants are viable but show defects in maintaining genome stability and are highly sensitive to ionizing radiation. Interestingly, mutating Dmchk2 completely blocks DNA damage-induced apoptosis and partially blocks DNA damage-induced cell cycle arrest. These results indicate that Chk2 protein plays a crucial role in the DNA damage response pathway mediating cell cycle arrest and apoptosis, and that the ATM-Chk2 pathway is likely conserved in Drosophila.
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Language of Publication	English
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Publication Type	Journal
Abbreviation	FEBS Lett.
Title	FEBS Letters
Publication Year	1968-
ISBN/ISSN	0014-5793
Data from Reference
Aberrations (1)
	Df(2L)E51
Alleles (8)
	barr^+tXa barr^E51 barr^k14014 grp⁰⁶⁰³⁴ lok^E51 lok^hs.PX mei-41^RT1 w^+mC
Constructs (2)
	P{barr^+tXa} P{hs-lok.X}
Genes (6)
	barr grp His3 lok mei-41 w
Insertions (1)
	P{lacW}barr^k14014