The Cln3/Cdc28 kinase is
required to activate the Swi4/Swi6 transcription complex and induce
transcription of CLN1 and CLN2 in late G1 which drive the transition
to S phase. SWI4 and CLN3 provide independent, rate-limiting functions
that affect the length of G1 and cell size. SWI4 and CLN3 are
transcriptionally regulated by elements referred to as ECBs (early
cell cycle boxes), which induce a wave of transcription at the M/G1
transition. To see if ECB-mediated transcription of CLN3 and SWI4
provides the coordinated burst of expression of these two rate
limiting gene products required to drive the transition to S phase, we
have constructed strains in which we have eliminated the ECB elements
from the CLN3 and/or SWI4 promoters (cln3ecb and swi4ecb) and assessed
the effects of these mutations upon G1 progression and size
control. Loss of ECB control of CLN3 and/or SWI4 results in cell
populations that are larger than wild type and spend more time in
G1. Daughter cells that are cln3ecb or swi4ecb mutants bud at a larger
cell size than wild type cells, but their behavior is still fairly
uniform and reproducible. In contrast, the cln3ecb swi4ecb double
mutant displays a highly variable budding profile which is
asynchronous and occurs over a very broad range of cell sizes. This is
consistent with the view that ECB-mediated transcription of CLN3 and
SWI4 provides the signal which determines the timing of the transition
to S phase.
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