Abstract

[Gregory May]

Mitotic Catastrophe is the Mechanism of Lethality 
for Mutations that Confer Mutagen 
Sensistivity in Aspergillus nidulans. 

Mutation Research 304:193-202 (1994)
 
Steven H. Denison and Gregory S. May 

Department of Cell Biology, Baylor 
College of Medicine, Houston, TX  77030 USA 
 
Summary 
	We have examined the consequences of treatment with DNA 
damaging agents of uvs mutants and the bimD6 mutant of Aspergillus 
nidulans.   We first established that wild Aspergillus undergoes 
a cell cycle delay following treatment with the DNA damaging 
agents methyl methanesulfonate (MMS) and ultraviolet light (UV).  
We have also determined that strains carrying the bimD6, uvsB110, 
uvsH77, uvsF201and the uvsC114 mutations, all of which cause an 
increased sensitivity to DNA-damaging agents, undergo a cell cycle 
delay following DNA damage.  These mutations do not therefore represent 
nonfunctional checkpoint mutations in Aspergillus.  However, all of the 
mutant strains accumulated nuclear defects after the period of delay 
following mutagen treatment.  The nuclear defects in the uvsB110 and 
bimD6 strains following MMS treatment were shown to be dependent on 
passage through mitosis after DNA damage, as the defects were 
prevented with benomyl.  Checkpoint controls responding to DNA 
damage are thus able to only temporarily halt cell cycle progression 
in response to DNA damage.  The conditional bimD6 mutation results in 
a defective mitosis at restrictive temperatures.  This mitotic defect 
is copied with MMS treatment at temperatures permissive for the mitotic 
defect.  The bimD gene product may perform a role in DNA repair which is 
also required in the mitotic cell cycle in the absence of damage due to 
mutagen treatment.   

gsmay at bcm.tmc.edu