Transcriptional Control of the Plant Cell Cycle 17
ent logic of control of CDK-dependent and ubiquitin-dependent mechanisms,
which requires phase specific transcription and accumulation of at least some
key regulators, it is very unlikely that it plays only a minor role.
1.1.2
Protein Phosphorylation in the Eukaryotic Cell Cycle
Heteromeric protein kinase complexes comprising various catalytic subunits
(CDK proteins) in obligate association with one of many distinct activating
cyclin subunits that accumulate and decay periodically in the course of the
cell cycle mediate major cell cycle transitions: at START, the commitment to
a cell cycle conditional on the determination of adequate cell mass; at G1/S,
the commitment to a round of nuclear DNA replication; at G2/M, the dissolu-
tion of the nuclear compartment; and at the metaphase to anaphase transition,
the irreversible separation of sister chromatids for segregation into two new
cells. The cyclin–CDK cycle has recently been reviewed, therefore, I shall focus
on the basic principles of CDK-dependent cell cycle regulation here and not
invest them with details (see Inzé and Veylder (2006) for an excellent recent re-
view of cell cycle control in plants, and Morgan (2007) for an outstanding and
comprehensive review of the principles of cell cycle regulation).
The key function of cyclin–CDK complexes in the cell cycle is to orches-
trate and decisively mediate progression through crucial control points. This
role is reflected in their regulation, which occurs in a series of primed steps
and culminates in a runaway, exponential increase of cyclin–CDK activity at
the onset of the relevant phase transition.
To exemplify this, I will discuss the processes in budding yeast during
G1 phase that lead up to the key cell cycle transition at G1/S in detail; our
understanding of the plant cell cycle, and of its biochemistry in particular,
is still too fragmentary to provide a comprehensive picture at the present
time. For those biological systems in which cells grow and accrue mass in
G1, which includes budding yeast and animal cells, but not fission yeast
(where growth occurs during G2), it is useful to consider G1 phase as two
distinct parts: In the first part, which commences as soon as cells have com-
pleted their exit from mitosis, control of cell cycle progression is ceded to
the mechanisms that assess cell mass. The mechanism by which cell growth
is measured in plants, and whether there is a single such mechanism in all
plants, is not clear yet. In budding yeast, these mechanisms are thought to re-
sult in the gradual accumulation of cyclin3 protein (Cln3p), proportional to
cell growth; culminating in the accumulation of sufficient Cln3p-CDK activity
to propel it into the next part of G1. This occurs by Cln3p-CDK phosphory-
lation of an inhibitor of the SBF transcription factor complex, which leads
to the inactivation of the inhibitor. As explained in the previous section,
SBF activity is central to the transcriptional network that launches S-phase.
In this second part of G1, different cyclin–CDK complexes take the reins to