Biology Reference
In-Depth Information
the Lov-1
FLC
allele requires a much longer period of cold to accumulate
high levels of H3K27me3 and achieve full
FLC
silencing. This extended
delay in flowering matches the longer winters encountered in northern
Europe. This work illustrates how chromatin-based mechanisms can be
modulated by a few changes in the regulatory sequences of a gene with
strong phenotypic impact and how epigenetic regulation can be linked to
adaptation.
Providing that plants have experienced cold for long enough, typically
several weeks, stable silencing of
FLC
is maintained and passed on through
mitosis during the rest of the life cycle, even when temperatures become
warmer. This epigenetic “memory of winter” requires the activity of the
PRC2-PHD complex that spreads H3K27me3 across the entire
FLC
locus
(
De Lucia et al., 2008
)(
Fig. 6.1
C). Association of PHD-PRC2 with an
additional PHD protein named VERNALIZATION INSENSITIVE3
(VIN3), the expression of which peaks at the end of the vernalization period,
appears essential to achieve stable silencing of
FLC
(
Heo & Sung, 2011;
Sung & Amasino, 2004
). Maintenance of
FLC
repression also relies on
LHP1 and AtBMI1C, two members of a PRC1-like complex (
Li et al.,
2011; Mylne et al., 2006; Sung et al., 2006
).
Mathematical modeling of the vernalization process has highlighted
general principles that might pertain to other chromatin-based “memory”
systems (
Angel, Song, Dean, & Howard, 2011; Satake & Iwasa, 2012;
Song, Angel, Howard, &Dean, 2012
). Akey feature is that cold-induced epi-
genetic silencing of
FLC
is cell-autonomous and bistable, that is, in each cell,
the locus can exist in one of the two stable states, active or silent. The switch is
probabilistic and relies on a positive feedback, whereby a local change (the
nucleation of H3K27me3) recruits catalytic activities (PRC2 and PRC1) that
reinforce this initial event and stabilize the silent state through cell division.
Another key feature is that the probability of this cell-autonomous switch
increases with the duration of the triggering signal (cold), thus providing a
biological measure of time based on the fraction of cells that have switched
(
Fig. 6.1
D). Experimental testing of this hypothesis indicates indeed that
the quantitative relationship between
FLC
repression and H3K27me3 accu-
mulation appears to act at the cell population level, with an increasing number
of cells in which
FLC
is silent resulting from longer cold exposure (
Angel
et al., 2011
). This population averaging strategy, which provides a means
to buffer noisy changes in the environment, likely contributes to the robust-
ness of the responsewhereby a license to flower is only granted by
FLC
silenc-
ing after winter has passed (
Satake & Iwasa, 2012; Song et al., 2012
).
