Abstract - Aspergillus cell cycle

Steven.W.James at JUPITER.CC.GETTYSBURG.EDU Steven.W.James at JUPITER.CC.GETTYSBURG.EDU
Sat Nov 11 12:58:23 EST 1995


James, Steven W.1,2 , Peter M. Mirabito1, Peter C.Scacheri2, and N. Ronald
Morris1.  
        1995.  The Aspergillus nidulans bimE (blocked-in-mitosis) gene
encodes multiple cell 
        cycle functions involved in mitotic checkpoint control and mitosis.
 Journal of Cell 
        Science 108:  3485-3499.

1Department of Pharmacology, University of Medicine and Dentistry of New
Jersey - Robert Wood Johnson Medical School, Piscataway, NJ  08854-5635

2Current address:  Department of Biology, Gettysburg, Gettysburg, PA  17325

 To whom correspondence should be addressed

SUMMARY
The bimE  (blocked-in-mitosis) gene appears to function as a negative
mitotic regulator because the recessive bimE7 mutation can override certain
interphase-arresting treatments and mutations, causing abnormal induction
of mitosis.  We have further investigated the role of bimE in cell cycle
checkpoint control by (1) coordinately measuring mitotic induction and DNA
content of bimE7 mutant cells, and (2) analyzing epistasis relationships
between bimE7 and 16 different nim mutations.  A combination of cytological
and flow cytometric techniques was used to show that  bimE7 cells at
restrictive temperature (44o C) undergo a normal, although somewhat slower
cell cycle prior to mitotic arrest.  Most bimE7 cells were fully reversible
from restrictive temperature arrest, indicating that they are able to enter
mitosis normally, and therefore require bimE function in order to finish
mitosis.  Furthermore, epistasis studies between bimE7 and mutations in
cdc2 pathway components revealed that the induction of mitosis caused by
inactivation of bimE  requires functional p34cdc2 kinase, and that mitotic
induction by bimE7 depends upon several other nim genes whose functions are
not yet known.  The involvement of bimE  in S phase function and mitotic
checkpoint control was suggested by three lines of evidence.  First, at
restrictive temperature the bimE7 mutation slowed the cell cycle by
delaying the onset or execution of S phase.  Second, at permissive
temperature (30o C) the bimE7 mutation conferred enhanced sensitivity to
the DNA synthesis inhibitor hydroxyurea.  Finally, the checkpoint linking M
phase to the completion of S phase was abolished when bimE7 was combined
with two nim mutations that cause arrest in G1 or S phase.  A model for
bimE function based on these findings is presented.



                Dr. Steven James
                Assistant Professor of Biology
                Department of Biology
                Gettysburg College
                Gettysburg, PA  17325

                Office: (717)-337-6170
                Fax:  (717)-337-6157
                e-mail:  sjames at cc.gettysburg.edu




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