Root Development and Abiotic Stress Adaptation - Abiotic Stress: Plant Responses and Applications in Agriculture - page 141

Cyclosome (APC/C), a Cullin-RING finger E3 ligase, is most active from the M phase to G1
phase. APC/C complex is composed by at least 11 subunits, and in the Arabidopsis genome,
all APC/C components except for APC3/CDC27/HOBBIT are encoded by a single gene [54].
All APC/C subunit mutants studied so far accumulate mitotic CYCs in embryo sacs, suggesting
that they're substrates of the APC/C [52, 54]. Apart from its core components, APC/C also pairs
with co-activators, known as CDC20/FIZZY and CDC20 HOMOLOG1 (CDH1)/FIZZY-
RELATED (FZR), which confer substrate specificity and are activated during distinct phases
of the cell cycle with equally distinct activities. The Arabidopsis genome contains five CDC20
and three CDH1 genes, also called CELL CYCLE SWITCH 52 (CCS52), and even if their
modification of the APC/C activity during the cell cycle is not fully established, CCS52A1 and
CCS52A2 participate in meristem maintenance [55]. Notably, they act through different
mechanisms and exhibit different expression patterns as well. The expression of CCS52A1
starts at the elongation zone of Arabidopsis roots and stimulates mitotic exit and an entry into
the endoreplication cycle, whereas CCS52A2 is expressed at the distal part of the root meristem
and is required to maintain the cell identity in the QC. The ccs52a2 mutation activates the QC
cell division, contrasting with the occasional division behavior normally presented, and when
its promoter is switched with the one of CCS52A1, the expression of the latter rescues the
phenotype in ccs52a2 , suggesting homologous function. In vertebrates, negative regulators also
modify the activity of APC/C. These regulators, called Early mitotic inhibitor1 (Emi1) and Emi2
directly bind to CCS52 and CDC20, inhibiting the APC/C activity. No direct plant orthologs
are identified, but recent studies have shown that GIGAS CELL1 (GIG1)/OMISSION OF
SECOND DIVISION 1 (OSD) and UV-INSENSITIVE4 (UVI4)/POLYCHROME (PYM) act as
their functional homologs in plants [56, 57] by physically interacting with the APC/C activators
CCS52 and CDC20. Their overexpression causes an accumulation of CYCB1;2 and CYCA2;3,
respectively, by the inactivation of the APC/C, suggesting that it also could have an effect on
root meristem maintenance by the inhibition of the APC/C-CCS52 complex activity. Another
important way to control and modulate the CYC-CDK complexes activity involves said
complexes binding directly to CDK inhibitors, proteins that interfere with the ability of CYC-
CDK to phosphorylate their substrates. Plants have two classes of CDK inhibitors - KIP-
RELATED PROTEINs (KRPs) and SIAMESE (SIM)/SIAMESE RELATED (SMR). The
Arabidopsis genome encodes 7 KRPs, KRP1-7, and at least 13 SIM/SMRs. Recent analyses have
shown that all 7 KRPs purify conjoined with CYCDs and CDKA [36] suggesting that they
inhibit the activity of the CYCD-CDKA complexes, as it has been proposed previously [58],
but not excluding the possibility of them inhibiting the activity of CYCD-CDKB complexes as
well [59]. The seven KRPs display overlapping but distinct expression patterns in the Arabi‐
dopsis shoot apex, some of them present strongly in dividing cells, like KRP4 and KRP5, while
KRP1 and KRP2 are present in differentiating cells [60]. KRPs have a role driving the endore‐
plication cycle as well, also by inhibiting CDK activities [61, 62]. The SIM/SMR family of CDK
inhibitors is found only in plants, and is required to repress the mitotic cell cycle in trichomes
via the interaction of SIM with the CYCD-CDKA complex [63]. Another member of the SIM
family, SMR1/LGO, is implicated in the control of endoreplication in sepals [64], maintaining
the presence of elongated, endoreplication-undergone giant cells in the sepals, which are lost
in the smr1/lgo because they progressed through additional cell divisions instead of endore‐