The continuous development of roots is supported by a sustainable system for cell production and growth at the root tip. In the stem cell niche that consists of a quiescent centre and surrounding stem cells, an undifferentiated state and low mitotic activity are preserved by the action of auxin and abscisic acid. Stem cell daughters divide several times in the proximal meristem, where auxin and gibberellin mainly promote cell proliferation. Cells then elongate with the help of gibberellin, and become finally differentiated as a constituent of a cell file in the elongation/differentiation zone. In the model plant Arabidopsis thaliana, the transition zone is located between the proximal meristem and the elongation/differentiation zone, and plays an important role in switching from mitosis to the endoreplication that causes DNA polyploidization. Recent studies have shown that cytokinins are essentially required for this transition by antagonizing auxin signalling and promoting degradation of mitotic regulators. In each root zone, different phytohormones interact with one another and coordinately control cell proliferation, cell elongation, cell differentiation, and endoreplication. Such hormonal networks maintain the elaborate structure of the root tip under various environmental conditions. In this review, we summarize and discuss key issues related to hormonal regulation of root growth, and describe how phytohormones are associated with the control of cell cycle machinery.
Inhibition of cell division is an active response to DNA damage that enables cells to maintain genome integrity. However, how DNA damage arrests the plant cell cycle is largely unknown. Here, we show that the repressor-type R1R2R3-Myb transcription factors (Rep-MYBs), which suppress G2/M-specific genes, are required to inhibit cell division in response to DNA damage. Knockout mutants are resistant to agents that cause DNA double-strand breaks and replication stress. Cyclin-dependent kinases (CDKs) can phosphorylate Rep-MYBs in vitro and are involved in their proteasomal degradation. DNA damage reduces CDK activities and causes accumulation of Rep-MYBs and cytological changes consistent with cell cycle arrest. Our results suggest that CDK suppressors such as CDK inhibitors are not sufficient to arrest the cell cycle in response to DNA damage but that Rep-MYB-dependent repression of G2/M-specific genes is crucial, indicating an essential function for Rep-MYBs in the DNA damage response.
Root growth is controlled by mechanisms underlying cell division and cell elongation, which respond to various internal and external factors. In Arabidopsis (), cells produced in the proximal meristem (PM) elongate and differentiate in the transition zone (TZ) and the elongation/differentiation zone (EDZ). Previous studies have demonstrated that endoreplication is involved in root cell elongation; however, the manner by which cells increase in length by more than 2-fold remains unknown. Here, we show that epidermal and cortical cells in Arabidopsis roots undergo two modes of rapid cell elongation: the first rapid cell elongation occurs at the border of the proximal meristem and the TZ, and the second mode occurs during the transition from the TZ to the EDZ. Our previous study showed that cytokinin signaling promotes endoreplication, which triggers the first rapid cell elongation. Our cytological and genetic data revealed that the second rapid cell elongation involves dynamic actin reorganization independent of endoreplication. Cytokinins promote actin bundling and the resultant second rapid cell elongation through activating the signaling pathway involving the cytokinin receptors ARABIDOPSIS HISTIDINE KINASE3 (AHK3) and AHK4 and the B-type transcription factor ARABIDOPSIS RESPONSE REGULATOR2. Our results suggest that cytokinins promote the two modes of rapid cell elongation by controlling distinct cellular events: endoreplication and actin reorganization.
SUMMARYCyclin-dependent kinases (CDKs) play an essential role in cell cycle regulation during the embryonic and postembryonic development of various organisms. Full activation of CDKs requires not only binding to cyclins but also phosphorylation of the T-loop domain. This phosphorylation is catalysed by CDK-activating kinases (CAKs). Plants have two distinct types of CAKs, namely CDKD and CDKF; in Arabidopsis, CDKF;1 exhibits the highest CDK kinase activity in vitro. We have previously shown that CDKF;1 also functions in the activation of CDKD;2 and CDKD;3 by T-loop phosphorylation. Here, we isolated the knockout mutants of CDKF;1 and showed that they had severe defects in cell division, cell elongation and endoreduplication. No defect was observed during embryogenesis, suggesting that CDKF;1 function is primarily required for post-embryonic development. In the cdkf;1 mutants, T-loop phosphorylation of CDKA;1, an orthologue of yeast Cdc2/Cdc28p, was comparable to that in wild-type plants, and its kinase activity did not decrease. In contrast, the protein level and kinase activity of CDKD;2 were significantly reduced in the mutants. Substitution of threonine-168 with a non-phosphorylatable alanine residue made CDKD;2 unstable in Arabidopsis tissues. These results indicate that CDKF;1 is dispensable for CDKA;1 activation but is essential for maintaining a steady-state level of CDKD;2, thereby suggesting the quantitative regulation of a vertebrate-type CAK in a plant-specific manner.
How cell size and number are determined during organ development remains a fundamental question in cell biology. Here, we identified a GRAS family transcription factor, called SCARECROW-LIKE28 (SCL28), with a critical role in determining cell size in Arabidopsis. SCL28 is part of a transcriptional regulatory network downstream of the central MYB3Rs that regulate G2 to M phase cell cycle transition. We show that SCL28 forms a dimer with the AP2-type transcription factor, AtSMOS1, which defines the specificity for promoter binding and directly activates transcription of a specific set of SIAMESE-RELATED (SMR) family genes, encoding plant-specific inhibitors of cyclin-dependent kinases and thus inhibiting cell cycle progression at G2 and promoting the onset of endoreplication. Through this dose-dependent regulation of SMR transcription, SCL28 quantitatively sets the balance between cell size and number without dramatically changing final organ size. We propose that this hierarchical transcriptional network constitutes a cell cycle regulatory mechanism that allows to adjust cell size and number to attain robust organ growth.
Leaf venation develops complex patterns in angiosperms, but the mechanism underlying this process is largely unknown. To elucidate the molecular mechanisms governing vein pattern formation, we previously isolated vascular network defective (van) mutants that displayed venation discontinuities. Here, we report the phenotypic analysis of van4 mutants, and we identify and characterize the VAN4 gene. Detailed phenotypic analysis shows that van4 mutants are defective in procambium cell differentiation and subsequent vascular cell differentiation. Reduced shoot and root cell growth is observed in van4 mutants, suggesting that VAN4 function is important for cell growth and the establishment of venation continuity. Consistent with these phenotypes, the VAN4 gene is strongly expressed in vascular and meristematic cells. VAN4 encodes a putative TRS120, which is a known guanine nucleotide exchange factor (GEF) for Rab GTPase involved in regulating vesicle transport, and a known tethering factor that determines the specificity of membrane fusion. VAN4 protein localizes at the trans-Golgi network/early endosome (TGN/EE). Aberrant recycling of the auxin efflux carrier PIN proteins is observed in van4 mutants. These results suggest that VAN4-mediated exocytosis at the TGN plays important roles in plant vascular development and cell growth in shoot and root. Our identification of VAN4 as a putative TRS120 shows that Rab GTPases are crucial (in addition to ARF GTPases) for continuous vascular development, and provides further evidence for the importance of vesicle transport in leaf vascular formation.
SUMMARYFor the full activation of cyclin-dependent kinases (CDKs), not only cyclin binding but also CDK phosphorylation is required. This activating phosphorylation is mediated by CDK-activating kinases (CAKs). Arabidopsis has four genes showing similarity to vertebrate-type CAKs, three CDKDs (CDKD;1-CDKD;3) and one CDKF (CDKF;1). We previously found that the cdkf;1 mutant is defective in post-embryonic development, even though the kinase activities of core CDKs remain unchanged relative to the wild type. This raised a question about the involvement of CDKDs in CDK activation in planta. Here we report that the cdkd;1 cdkd;3 double mutant showed gametophytic lethality. Most cdkd;1-1 cdkd;3-1 pollen grains were defective in pollen mitosis I and II, producing one-cell or two-cell pollen grains that lacked fertilization ability. We also found that the double knock-out of CDKD;1 and CDKD;3 caused arrest and/or delay in the progression of female gametogenesis at multiple steps. Our genetic analyses revealed that the functions of CDKF;1 and CDKD;1 or CDKD;3 do not overlap, either during gametophyte and embryo development or in post-embryonic development. Consistent with these analyses, CDKF;1 expression in the cdkd;1-1 cdkd;3-1 mutant could not rescue the gametophytic lethality. These results suggest that, in Arabidopsis, CDKD;1 and CDKD;3 function as CAKs controlling mitosis, whereas CDKF;1 plays a distinct role, mainly in post-embryonic development. We propose that CDKD;1 and CDKD;3 phosphorylate and activate all core CDKs, CDKA, CDKB1 and CDKB2, thereby governing cell cycle progression throughout plant development.
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