Agriculture Reference
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very limited. However, there have been identified several key players in stress-induced cell
cycle modifications that have cast the first light over the understanding the talk between
environmental signals and the mitotic or endoreplication cycle. Gibberellins (GAs), plant
hormones, promote cell expansion by disrupting growth inhibitory proteins named DELLAs
[156] and also promote cell proliferation in Arabidopsis [157]. In the root meristem of GA-
deficient mutants, cell division rate is decreased and the phenotype is rescued by GA treat‐
ment. DELLA proteins are also involved in this regulation, as non-degradable forms of DELLA
inhibit cell proliferation. Low levels of GAs in GA-deficient mutants enhance the expression
of certain CDK inhibitor genes - KRP2, SIM, SMR1 and SMR2- with a DELLA-related mech‐
anism, and cell proliferation defects shown by these mutants can be recovered by overex‐
pressing CYCD3;1. These findings tend to indicate that GA signaling drives cell proliferation
by modulating the activity of CYC-CDK complexes, at least partially mediated by the DELLA-
dependent expression of CDK inhibitors, and thus making DELLA a potential intermediate in
the signal transduction channel connecting environmental signals and cell cycle progression.
This is proposed to be a consequence of reduced cell expansion and associated division of the
endodermis layer in the root apical meristem [158, 159], suggesting a role for the endodermis
in controlling the growth rate in the root apical meristem. Another potential link is RICE SALT
SENSITIVE 1 (RSS1), controlling the cell cycle progression under various abiotic stress
conditions [160]. The
rss1
mutants do not present evident growth defects under normal
conditions, but they display hypersensitivity to high salinity, ionic stress and hyperosmotic
stress. Under these conditions, in
rss1
, shoot and root meristems are severely affected, showing
a reduced population of proliferating cells, leaving RSS1 as a required factor for proliferative
cell status in the meristem. RSS1 is expressed during the S phase of the mitotic cycle and its
protein is degraded via APC/C during the M/G1 transition. RSS1 interacts with a Type 1 Protein
Phosphatase (PP1), known in humans to inactivate Retinoblastoma (Rb) proteins through
dephosphorylation, which is inhibitory to the G1/S transition [161]. Sugars can act as signaling
molecules in assorted biological processes, and even that sucrose-dependent cyclin expression
is known since a decade ago [162], LR formation through sucrose induction is a good example
of sugar-dependent reactivation of cell proliferation [163]. This recent study shows that the
expression of CYCD4;1 levels in root pericycle cells is dependent on the sucrose availability,
and that reduced CYCD4;1 levels in
cyca4;1
mutants or wild-type (wt) roots grown in the
absence of sucrose cause LR density to drop. It is not clear how sucrose upregulates CYCD4;1
in specifically in that kind of cells, but these findings suggest that the transcriptional effect has
to do with sucrose-dependent regulation of LR density. Notably, auxin does not have an effect
over the expression of CYCD4;1 in pericycle cells, and restores the reduced LR density
phenotype of cyca4;1 mutants, suggesting that CYCD4;1 has no role in the auxin-mediated LR
initiation pathway. CYCD3;1, is also responsive to sucrose availability, but the effects of this
over CYCD3;1 activities are not clear [164]. Endoreplication progress is also affected by several
environmental signals. E2F3/ DEL1, an atypical E2F present in Arabidopsis, and that functions
as a transcriptional repressor, is one of the key regulators that negatively controls the entry
into the endoreplicative cycle [165]. It has been suggested that the balance between the
transcriptional activator E2Fb and repressor E2Fc controls light-dependent endoreplication
through the antagonistic modification of the DEL1 expression [166]. E2Fb and E2Fc compete
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