Linked Life Data

7614481

Source:http://linkedlifedata.com/resource/pubmed/id/7614481

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
1995-8-22
pubmed:abstractText
Three Mitomycin C (MMC)-hypersensitive mutants (CL-V1B, CL-V5B, and CL-V101B) were isolated from Chinese hamster V79B cells by the replica plating technique. In comparison to the parental cell line, CL-V1B, CL-V5B, and CL-V101B show about a 22-, 32-, and 13-fold increased sensitivity to MMC, respectively (judged by the D10). These mutants are also sensitive to other DNA cross-linking agents, such as 1,2,3,4-diepoxybutane (9-, 19-, and 12-fold, respectively) and cis-diamminedichloroplatinum(II) (17-, 12-, and 6-fold, respectively). CL-V5B and CL-V101B display an exclusive sensitivity to DNA cross-linking agents, whereas CL-V1B also shows an increased sensitivity to monofunctional alkylating agents, such as methyl methanesulfonate (3-fold) and ethyl methanesulfonate (2-fold), and UV254mm (2-fold). Approximately 2-3-fold higher levels of spontaneous chromosomal aberrations are found in these three mutants in comparison to wild-type V79B cells. At a MMC survival level of 80%, CL-V5B demonstrates a 16-fold higher level of MMC-induced chromosomal damage than V79B. Despite phenotypical heterogeneity within this group of mutants, hybrid clones derived after fusion remained MMC sensitive, indicating that these mutants belong to the same complementation group. To determine whether the mutants represent a new complementation group among other Chinese hamster cell mutants that also display hypersensitivity to MMC, CL-V1B cells were fused with mutants representing different complementation groups i.e., irs1, irs3, irs1SF, UV20, UV41, V-H4, and V-C8 cells. In all cases, the derived hybrids regained MMC sensitivity similar to wild-type cells, indicating that the CL-V1B mutant represents a new complementation group. The phenotype of CL-V1B, CL-V5B, and CL-V101B cells closely resembles the phenotype of Fanconi anemia cells, suggesting that these hamster mutants could be defective in a gene that is involved in this disorder.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3412-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
A new complementation group of mitomycin C-hypersensitive Chinese hamster cell mutants that closely resembles the phenotype of fanconi anemia cells.
pubmed:affiliation
Department of Radiation Genetics and Chemical Mutagenesis, Leiden University, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't