Sb. Helliwell et al., TOR2 IS PART OF 2 RELATED SIGNALING PATHWAYS COORDINATING CELL-GROWTHIN SACCHAROMYCES-CEREVISIAE, Genetics, 148(1), 1998, pp. 99-112
The Saccharomyces cerevisiae genes TORI and TOR2 encode phosphatidylin
ositol kinase homologs. TOR2 has two essential functions. One function
overlaps TOR1 and mediates protein synthesis and cell cycle progressi
on. The second essential function of TOR2 is unique to TOR2 and mediat
es the cell-cycle-dependent organization of the actin cytoskeleton. We
have isolated temperature-sensitive mutants that are defective for ei
ther one or both of the two TOR2 functions. The three classes of mutan
ts were as follows. Class A mutants, lacking only the TOR2-unique func
tion, are defective in actin cytoskeleton organization and arrest with
in two to three generations as small-budded cells in tile G2/M phase o
f the cell cycle. Class B mutants, lacking only the TOR-shared functio
n, and class C mutants, lacking both functions, exhibit a rapid loss o
f protein synthesis and a G1 arrest within one generation. To define f
ur-ther-the two functions of TOR2, we isolated multicopy suppressors t
hat rescue the class A or B mutants. Overexpression of MSS4, PKC1, PLC
1, RHO2, ROM2, or SUR1 suppressed the growth defect of a class A mutan
t. Surprisingly, overexpression of PLC1 and MSS4 also suppressed the g
rowth defect of a class B mutant. These genes encode proteins that are
involved in phosphoinositide metabolism and signaling. Thus, the two
functions (readouts) of TOR2 appear to involve two related signaling p
athways controlling cell growth.