The fission yeast minichromosome loss mutant mcl1-1 was identified in a screen 
for mutants defective in chromosome segregation. Missegregation of the 
chromosomes in mcl1-1 mutant cells results from decreased centromeric cohesion 
between sister chromatids. mcl1+ encodes a beta-transducin-like protein with 
similarity to a family of eukaryotic proteins that includes Ctf4p from 
Saccharomyces cerevisiae, sepB from Aspergillus nidulans, and AND-1 from humans. 
The previously identified fungal members of this protein family also have 
chromosome segregation defects, but they primarily affect DNA metabolism. 
Chromosomes from mcl1-1 cells were heterogeneous in size or structure on 
pulsed-field electrophoresis gels and had elongated heterogeneous telomeres. 
mcl1-1 was lethal in combination with the DNA checkpoint mutations rad3delta and 
rad26delta, demonstrating that loss of Mcl1p function leads to DNA damage. 
mcl1-1 showed an acute sensitivity to DNA damage that affects S-phase 
progression. It interacts genetically with replication components and causes an 
S-phase delay when overexpressed. We propose that Mcl1p, like Ctf4p, has a role 
in regulating DNA replication complexes.