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J. Cell Biol.,
Volume 144, Number 1, January 11, 1999 71-82
Institute of Molecular and Cell Biology, National University of Singapore, Singapore 117609
Normal actin cytoskeleton organization in
budding yeast requires the function of the Pan1p/
End3p complex. Mutations in PAN1 and END3 cause
defects in the organization of actin cytoskeleton and
endocytosis. By screening for mutations that can suppress the temperature sensitivity of a pan1 mutant
(pan1-4), a novel serine/threonine kinase Prk1p is now
identified as a new factor regulating the actin cytoskeleton organization in yeast. The suppression of pan1-4 by
prk1 requires the presence of mutant Pan1p. Although viable, the prk1 mutant is unable to maintain an asymmetric distribution of the actin cytoskeleton at 37°C.
Consistent with its role in the regulation of actin cytoskeleton, Prk1p localizes to the regions of cell growth
and coincides with the polarized actin patches. Overexpression of the PRK1 gene in wild-type cells leads to lethality and actin cytoskeleton abnormalities similar to
those exhibited by the pan1 and end3 mutants. In vitro
phosphorylation assays demonstrate that Prk1p is able
to phosphorylate regions of Pan1p containing the
LxxQxTG repeats, including the region responsible for
binding to End3p. Based on these findings, we propose
that the Prk1 protein kinase regulates the actin cytoskeleton organization by modulating the activities of
some actin cytoskeleton-related proteins such as
Pan1p/End3p.
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