Ref ID: 18367
Author:
S.L. McGuire Anglin , T. Banta , C. Coile , C. Dixit , S. Eastlack , A.
Giang , J. Kobie , M. Nguyen , K. Shingler , A. Orzechowski , and S. James . Millsaps College, Jackson, MS
Author address:
Gettysburg College, Gettysburg, PA.
mcguisl@millsaps.edu
Full conference title:
Asperfest 8
Abstract:
The snxA1 cold-sensitive mutation of A. nidulans was originally identified as an extragenic suppressor of the nimX2 heat sensitive mutation. Analysis
F223L
of double mutants showed that snxA1 suppresses all three heat sensitive nimX mutations as well as mutations in nimE and nimT ; thatsnxA1
CDC2 CYCLINB CDC25
has a synthetic phenotype in combination with a deleted ankA ; and that snxA1 is not a general cell cycle suppressor. Western blot data suggest that
WEE1
the levels of both NIMX and CYCLINB are not affected by the snxA1 mutation. We have recently cloned snxA and found that it encodes a homolog of
Saccharomyces cerevisiae Hrb1, a protein involved in mRNA transcription and export. SNXA is nonessential; however, deletion of snxA results in an
extremely cold-sensitive phenotype similar to but more extreme than the snxA1 mutation; deletion also suppresses nimX mutations. Overexpression
CDC2
of wild-type SNXA complements snxA1. These data suggest that nonmutant SNXA functions to restrain NIMX/CYCLINB activity. GFP-labelled SNXA
localizes to the nucleus in 87% of germlings when grown at 29 C; 13% of germlings have no detectable SNXA. Studies are currently underway to
o
determine if SNXA localization correlates with CYCLINB localization. Funding provided by NIH NCRR P20RR016476 and NIH2R15GM055885
Abstract Number: 45)
Conference Year: 2011
Link to conference website: NULL
New link: NULL
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Title
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Year
Number
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40
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39
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v
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32
n/a