Root Development and Abiotic Stress Adaptation - Abiotic Stress: Plant Responses and Applications in Agriculture - page 142

plication. Recent studies [34] show that both SIM and SMR/LGO are purified jointly with
CDKB1;1 while other SMRs interact with CDKA;1, thus suggesting that CDKB1;1 could be
directly inhibited by SIM/SMR1 leading to endoreplication onset.
3.1.3. Cell cycle control in post-embryonic root development
The cell cycle relies not only on its own molecular machinery to determine cellular fate. Post-
embryonic plant development needs a highly precise coordination of cell cycle-directed
signaling to correctly drive cells to form new tissues or cell types, as is evident in root develop‐
ment. Molecular genetic studies have uncovered several key regulators involved in developmen‐
tal cell cycle control, and many of them have shown to be transcriptional regulators, but how are
they linked to cell cycle control has not been well characterized. SHORTROOT (SHR) and
SCARECROW (SCR) are members of the GRAS family of transcription factors required for the
asymmetric division of cortex/endodermis initial cells (CEI) in the root apical meristem [65, 66].
This tissue-formative division generates two new cellular kinds- cortex and endodermis, making
the CEI cell division control a key requisite for a proper root development. It has been demon‐
strated that both SHR and SCR directly regulate the expression of CYCD6;1, present at G1 and
S phases, by binding to its promoter [67]. CYCD6;1 is expressed specifically in CEI and CEI
daughter cells, and the asymmetric division of CEI is significantly decreased in the cycd6;1
mutants. Additionally, when CYCD6;1 is expressed ectopically in the shr mutant background,
it partially compensates the division defects presented by the latter, supporting the idea of
CYCD6;1 being downstream of the SHR/SCR pathway. Other cell cycle genes, like CDKB2;1 and
CDKB2;2, have their expression regulated by SHR and SCR, and when these CDKs are overex‐
pressed in endodermal cells, the formative cell division of the CEI is promoted. However, they
do not appear to be direct targets of SHR and SCR, implying that the activation of these CDK
genes is linked by another control factor. Cell proliferation needs to be restored in the xylem-
pericycle cells for the LR initiation and this process can be induced by auxin in many plant species,
like Arabidopsis. LR development starts by the degradation of INDOLE ACETIC ACID
14(IAA14)/ SOLITARY-ROOT (SLR), dependent on auxin, that leads to the de-repression of two
related AUXIN RESPONSE FACTORs (ARFs), ARF7 and ARF19 [68]. These ARFs are re‐
quired for the subsequent expression of LATERAL ORGAN BOUNDARIES 18 (LBD18] and
LBD33 transcription factors, which form a LBD18-LBD33 heterodimer that activates the
expression of the E2Fa, one of the E2F genes induced at LR initiation, by binding directly to its
promoter [69]. E2Fa expression is increased by auxin treatment at the LR initiation site and this
auxin-dependent E2Fa expression is lost in the iaa14/slr-1 mutant background. Expectedly, the
number of LR primordial is decreased in the e2fa mutants, evidencing a requirement of E2Fa for
LR emerging and establishing a link between auxin signaling and cell cycle progression during
LR development. Another unrelated pathway that is also involved in the auxin-induced LR
formation has KRP2 downregulated by auxin [70]. Under low auxin conditions, the CYCD2;1-
CDKA activity is repressed by the presence of KRP2. Upon auxin treatment, both gene expres‐
sion and protein accumulation of KRP2 is reduced, leading to an increase in the CYCD2;1-
CDKA activity and subsequent enhancement of LR induction. A possible hyperphosphorylation
of RBR resulting in the activation of E2Fb directly caused by the CYCD2;1-CDKA complex activity
has been suggested [69]. A model on the basis of available information on the density and