Welcome! Click here to login or here to register.
 |
|||||||||||||||||||
|
|||||||||||||||||||
 |
|||||||||||||||||||
"DNA ligase I is required for fetal liver erythropoiesis but is not essential for mammalian cell viability." |
Bentley D, Selfridge J, Millar JK, Samuel K, Hole N, Ansell JD, Melton DW |
Published Aug. 1, 1996 in Nat Genet volume 13 .
Pubmed ID: 8696349
Abstract:
| Four distinct DNA ligase activities (I-IV) have been identified within mammalian cells. Evidence has indicated that DNA ligase I is central to DNA replication, as well as being involved in DNA repair processes. A patient with altered DNA ligase I displayed a phenotype similar to Bloom's syndrome, being immunodeficient, growth retarded and predisposed to cancer. Fibroblasts isolated from this patient (46BR) exhibited abnormal lagging strand synthesis and repair deficiency. It has been reported that DNA ligase I is essential for cell viability, but here we show that cells lacking DNA ligase I are in fact viable. Using gene targeting in embryonic stem (ES) cells, we have produced DNA ligase I-deficient mice. Embryos develop normally to mid-term when haematopoiesis usually switches to the fetal liver. Thereupon acute anaemia develops, despite the presence of erythroid-committed progenitor cells in the liver. Thus DNA ligase I is required for normal development, but is not essential for replication. Hence a previously unsuspected redundancy must exist between mammalian DNA ligases. |
This publication refers to following REPAIRtoire entries:
| Genes |
Last modification of this entry: Oct. 6, 2010
Add your own comment!
There is no comment yet.
|
|
|
|