NDLI: CHL1 is a nuclear protein with an essential ATP binding site that exhibits a size-dependent effect on chromosome segregation

Content Provider	PubMed Central
Author	Holloway, Sandra L.
Copyright Year	2000
Abstract	Saccharomyces cerevisiae chl1 mutants have a significant increase in the rate of chromosome missegregation. CHL1 encodes a 99 kDa predicted protein with an ATP binding site consensus, a putative helix–turn–helix DNA binding motif, and homology to helicases. Using site-directed mutagenesis, I show that mutations that are predicted to abolish ATP binding in CHL1 inactivate its function in chromosome segregation. Furthermore, overexpression of these mutations interferes with chromosome transmission of a 125 kb chromosome fragment in a wild-type strain. Polyclonal antibodies against CHL1 show that CHL1 is predominantly in the nuclear fraction of S.cerevisiae. CHL1 function is more critical for the segregation of small chromosomes. In chl1Δ1/chl1Δ1 mutants, artificial circular or linear chromosomes <150 kb in size exhibit near random segregation (0.12 per cell division), whereas all chromosomes tested >225 kb were lost at rates (5 × 10–3 per cell division) comparable to that observed for endogenous chromosome III. These results reveal an important role for ATPases/DNA helicases in chromosome segregation. Such enzymes may alter DNA topology to allow loading of proteins involved in maintaining sister chromatid cohesion.
Starting Page	3056
File Format	PDF
ISSN	13624962
e-ISSN	13624962
Journal	Nucleic Acids Research
Issue Number	16
Volume Number	28
Language	English
Publisher	Oxford University Press
Publisher Date	2000-08-15
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Genetics

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