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Blood, Vol. 95 No. 12 (June 15), 2000:
pp. 3970-3977
Posttranscriptional cell cycle-dependent regulation of human
FANCC expression
Michael C. Heinrich,
Kirsten V. Silvey,
Stacie Stone,
Amy J. Zigler,
Diana J. Griffith,
Michelle Montalto,
Lin Chai,
Yu Zhi, and
Maureen E. Hoatlin
From the Department of Medicine, Division of Hematology and Medical
Oncology, Oregon Health Sciences University and Portland Veterans
Affairs Medical Center, Portland, OR.
The Fanconi Anemia (FA) Group C complementation group gene
(FANCC) encodes a protein, FANCC, with a predicted
Mr of 63000 daltons. FANCC is found in both the cytoplasmic
and the nuclear compartments and interacts with certain other FA
complementation group proteins as well as with non-FA proteins. Despite
intensive investigation, the biologic roles of FANCC and of the other
cloned FA gene products (FANCA and FANCG) remain unknown. As an
approach to understanding FANCC function, we have studied the molecular regulation of FANCC expression. We found that although FANCC
mRNA levels are constant throughout the cell cycle, FANCC is
expressed in a cell cycle-dependent manner, with the lowest levels seen in cells synchronized at the G1/S boundary and the highest levels in
the M-phase. Cell cycle-dependent regulation occurred despite deletion
of the 5' and 3' FANCC untranslated regions, indicating that information in the FANCC coding sequence is sufficient to mediate
cell cycle-dependent regulation. Moreover, inhibitors of proteasome
function blocked the observed regulation. We conclude that FANCC
expression is controlled by posttranscriptional mechanisms that are
proteasome dependent. Recent work has demonstrated that the functional
activity of FA proteins requires the physical interaction of at least
FANCA, FANCC, and FANCG, and possibly of other FA and non-FA proteins.
Our observation of dynamic control of FANCC expression by the
proteasome has important implications for understanding the molecular
regulation of the multiprotein complex.
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