Plants exhibit a unique developmental flexibility to ever-changing environmental conditions. To achieve their profound adaptability, plants are able to maintain permanent stem cell populations and form new organs during the entire plant life cycle. Signaling substances, called plant hormones, such as auxin, cytokinin, abscisic acid, brassinosteroid, ethylene, gibberellin, jasmonic acid, and strigolactone, govern and coordinate these developmental processes. Physiological and genetic studies have dissected the molecular components of signal perception and transduction of the individual hormonal pathways. However, over recent years it has become evident that hormones do not act only in a linear pathway. Hormonal pathways are interconnected by a complex network of interactions and feedback circuits that determines the final outcome of the individual hormone actions. This raises questions about the molecular mechanisms underlying hormonal cross talk and about how these hormonal networks are established, maintained, and modulated throughout plant development.
The endocycle represents an alternative cell cycle that is activated in various developmental processes, including placental formation, Drosophila oogenesis, and leaf development. In endocycling cells, mitotic cell cycle exit is followed by successive doublings of the DNA content, resulting in polyploidy. The timing of endocycle onset is crucial for correct development, because polyploidization is linked with cessation of cell division and initiation of terminal differentiation. The anaphase-promoting complex/cyclosome (APC/C) activator genes CDH1, FZR, and CCS52 are known to promote endocycle onset in human, Drosophila, and Medicago species cells, respectively; however, the genetic pathways governing development-dependent APC/C CDH1/FZR/CCS52 activity remain unknown. We report that the atypical E2F transcription factor E2Fe/DEL1 controls the expression of the CDH1/FZR orthologous CCS52A2 gene from Arabidopsis thaliana. E2Fe/DEL1 misregulation resulted in untimely CCS52A2 transcription, affecting the timing of endocycle onset. Correspondingly, ectopic CCS52A2 expression drove cells into the endocycle prematurely. Dynamic simulation illustrated that E2Fe/DEL1 accounted for the onset of the endocycle by regulating the temporal expression of CCS52A2 during the cell cycle in a development-dependent manner. Analogously, the atypical mammalian E2F7 protein was associated with the promoter of the APC/C-activating CDH1 gene, indicating that the transcriptional control of APC/C activator genes by atypical E2Fs might be evolutionarily conserved.D uring the mitotic cell cycle, DNA that is duplicated during the S phase is divided at the M phase, so that each daughter cell produced has a genomic DNA content equal to that of its parents. In contrast, during the endoreduplication cycle, no cytokinesis occurs between rounds of DNA replication, resulting in successive doublings of the DNA ploidy level. This process occurs in a wide variety of cell types in arthropods and mammals and is particularly prominent in dicotyledonous plants (1), especially in species with a small genome and a short life cycle, in which repetitive DNA replication might support growth under conditions that require rapid development (2, 3).Mitotic cell cycle progression and endoreduplication are linked events. Premature or delayed exit from the cell division program results in an increased or decreased DNA ploidy, respectively (4-10). Therefore, the onset of endoreduplication must be controlled precisely. At the molecular level, endoreduplication is likely achieved through elimination of the components needed to progress through mitosis (11). Predominant roles in this process are played by the anaphase-promoting complex/cyclosome (APC/C) activator genes, such as CDH1, FZR, and CCS52A, which have been found to promote endocycle onset and progression in human, Drososphila melanogaster, and Medicago truncatula cells, respectively (12-17). The mechanisms controlling the transcriptional activity of these genes remain unclear, however.Over the years, it has beco...
SUMMARYGravitropism aligns plant growth with gravity. It involves gravity perception and the asymmetric distribution of the phytohormone auxin. Here we provide insights into the mechanism for hypocotyl gravitropic growth. We show that the Arabidopsis thaliana PIN3 auxin transporter is required for the asymmetric auxin distribution for the gravitropic response. Gravistimulation polarizes PIN3 to the bottom side of hypocotyl endodermal cells, which correlates with an increased auxin response at the lower hypocotyl side. Both PIN3 polarization and hypocotyl bending require the activity of the trafficking regulator GNOM and the protein kinase PINOID. Our data suggest that gravity-induced PIN3 polarization diverts the auxin flow to mediate the asymmetric distribution of auxin for gravitropic shoot bending.
Plant organs originate from meristems where stem cells are maintained to produce continuously daughter cells that are the source of different cell types. The cell cycle switch gene CCS52A, a substrate specific activator of the anaphase promoting complex/ cyclosome (APC/C), controls the mitotic arrest and the transition of mitotic cycles to endoreduplication (ER) cycles as part of cell differentiation. Arabidopsis, unlike other organisms, contains 2 CCS52A isoforms. Here, we show that both of them are active and regulate meristem maintenance in the root tip, although through different mechanisms. The CCS52A1 activity in the elongation zone of the root stimulates ER and mitotic exit, and contributes to the border delineation between dividing and expanding cells. In contrast, CCS52A2 acts directly in the distal region of the root meristem to control identity of the quiescent center (QC) cells and stem cell maintenance. Cell proliferation assays in roots suggest that this control involves CCS52A2 mediated repression of mitotic activity in the QC cells. The data indicate that the CCS52A genes favor a low mitotic state in different cell types of the root tip that is required for meristem maintenance, and reveal a previously undescribed mechanism for APC/C mediated control in plant development.CDH1 ͉ cell differentiation ͉ endoreduplication ͉ quiescent center ͉ stem cells P lant growth and development depend on the persistent activity of meristems, allowing continuous postembryonic organogenesis. In the root tip, meristem maintenance is controlled by different mechanisms that involve the maintenance of stem cells in the root meristem (RM) and spatial control over mitotic exit at the RM-elongation zone (EZ) border.In the distal RM, stem cells are maintained in an undifferentiated state by the quiescent center (QC) cells (1). The QC represents a center of mitotic inactive cells resting in an extended G 1 phase (2). The stem cells around the QC divide according to strict spatial rules, and provide cell progenies that detach from the QC and differentiate into different root cell types (3). The auxin-PLETHORA (PLT) pathway provides positional information to set up the QC and surrounding stem cells whose activities depend on WOX5 and SHORT ROOT (SHR)-SCARECROW (SCR) transcription factors (4-7).As cells reach the RM-EZ border, they start to expand and terminally differentiate. Recently, it has been demonstrated that the spatial boundary of the RM and EZ is controlled by the rate of meristematic cell differentiation at this border (8). The transition involves exit from the mitotic cycle to the endocycle (9). In eukaryotes, endoreduplication (ER) onset requires inhibition of mitotic cyclin-dependent kinase (cdk) activities (10-12). This inhibition can be achieved by multiple mechanisms, but mostly by the degradation of mitotic cyclins by the anaphase promoting complex/cyclosome (APC/C) (13-15). The APC/C is an ubiquitin ligase that regulates cell cycle progression from metaphase to S phase by targeted degradation of numerous ce...
Lateral root (LR) formation is initiated when pericycle cells accumulate auxin, thereby acquiring founder cell (FC) status and triggering asymmetric cell divisions, giving rise to a new primordium. How this auxin maximum in pericycle cells builds up and remains focused is not understood. We report that the endodermis plays an active role in the regulation of auxin accumulation and is instructive for FCs to progress during the LR initiation (LRI) phase. We describe the functional importance of a PIN3 (PIN-formed) auxin efflux carrier-dependent hormone reflux pathway between overlaying endodermal and pericycle FCs. Disrupting this reflux pathway causes dramatic defects in the progress of FCs towards the next initiation phase. Our data identify an unexpected regulatory function for the endodermis in LRI as part of the fine-tuning mechanism that appears to act as a check point in LR organogenesis after FCs are specified. The EMBO Journal (2013) Beeckman et al, 2001). This new root developmental program initiates when a restricted number of pericycle cells overlaying the xylem pole acquire founder cell (FC) identity and divide asymmetrically. Next, these pericycle derived initials undergo a sequence of cell divisions and differentiation events that ultimately results in the formation of an LR primordium. The new organ will eventually emerge through the overlaying cell layers of the primary root and form a new apical meristem that will control further growth of the mature LR (Malamy and Benfey, 1997;Swarup et al, 2008).Accumulation of the plant hormone auxin in a restricted number of pericycle cells is one of the earliest events during FC specification that precedes LR initiation (LRI) (Dubrovsky et al, 2008). Interference with the auxin accumulation by chemical or genetic inhibition of auxin transport or downstream auxin responses leads to severe defects in FC establishment and LRI (Casimiro et al, 2001;Fukaki et al, 2002;Benková et al, 2003;Dharmasiri et al, 2005;Vanneste et al, 2005).Several studies have addressed the auxin-based mechanism that regulates recurrent LRI. The observation that a periodic auxin response in the protoxylem of the basal meristem later coincides with the site of LRI led to the hypothesis that FCs are primed before auxin accumulation occurs in the defined pericycle cells (De Smet et al, 2007). Similar studies based on the oscillating behaviour of the auxin response marker DR5:LUC further suggested that regular fluctuations in auxin response along with complex oscillating gene expression patterns which determine competence for LRI, are required for specification of root branching sites (Moreno-Risueno et al, 2010). Other work proposed that auxin accumulation in the FC pericycle cells might result from gravitropic root bending and/or mechanical changes acting on expression of auxin carriers such as AUX1 (Laskowski et al, 2008). Indeed, the correlation between primary root gravity responses and LRI suggested that they are co-regulated and that root waving promotes an alternating left-right L...
Plant cytokinesis deploys a transport system that centers cell plateforming vesicles and fuses them to form a cell plate. Here we show that the adaptin-like protein TPLATE and clathrin light chain 2 (CLC2) are targeted to the expanding cell plate and to the equatorial subregion of the plasma membrane referred to as the cortical division zone (CDZ). Bimolecular fluorescence complementation and immunodetection indicates that TPLATE interacts with clathrin. Pharmacological tools as well as analysis of protein targeting in a mutant background affecting cell plate formation allowed to discriminate two recruitment pathways for TPLATE and CLC2. The cell plate recruitment pathway is dependent on phragmoplast microtubule organization and the formation and transport of secretory vesicles. The CDZ recruitment pathway, on the other hand, is activated at the end of cytokinesis and independent of transGolgi-derived vesicle trafficking. TPLATE and CLC2 do not accumulate at a narrow zone central of the CDZ. We have dubbed this subdomain the cortical division site and show that it corresponds precisely with the position where the cell plate merges with the parental wall. These data provide evidence that the plasma membrane is subject to localized endocytosis or membrane remodeling processes that are required for the fusion of the cell plate with a predefined region of the plasma membrane.ytokinesis in plants, in contrast to that process in animals and yeasts, starts with targeted secretion and fusion of vesicles between the separated chromosomes at the center of the cell (1, 2). During the initial phases of plant cytokinesis, syntaxinmediated vesicle fusion, together with callose biosynthesis within the fused vesicles, creates a transient membrane compartment at the central plane of the phragmoplast microtubules (2). After this initial stationary phase of cytokinesis, de novo microtubule formation at the outer border, together with depolymerization of microtubules at the center, allows the centrifugal expansion and guidance of the cell plate toward the parental cell wall (3). Animal cells, but also yeasts, which, like plant cells, are enwound in a polysaccharide wall, use a contractile actin ring that pulls in the plasma membrane (PM) at the division plane by means of an acto-myosin-based mechanism that involves the formation of a cleavage furrow (4). This centripetal narrowing of the division plane reaches a final point when the remaining gap is closed by means of syntaxin-mediated membrane fusion, a process that was designated as abscission (5).Very little is known about membrane trafficking at the end of eukaryotic cytokinesis (6, 7). In plants, this involves the connection of the cell plate with the parental plasma membrane and the maturation of the cell plate into a cell wall. Electron microscopic and mutant analysis revealed multiple finger-like fusion tubes mediating cell plate anchoring and the importance of a timely deposition of callose (2, 8).TPLATE, a plant-specific protein with similarity to the Adaptin/ Coatomer pr...
Eukaryotic cells have developed different mechanisms to establish the division plane. In plants, the position is determined before the onset of mitosis by the preprophase band (PPB). This ring of microtubules surrounds the nucleus and disappears completely by prometaphase. An unknown marker is left behind by the PPB, providing the necessary spatial cues during cytokinesis. At the position of the PPB, cortical actin is removed or modified to generate an actin-depleted zone that was proposed to provide the structural means for phragmoplast guidance. Here, we identify a plasma membrane domain that emerges at the onset of mitosis and persists until the end of cytokinesis. The narrow band in the plasma membrane corresponds to the position of the PPB and is prevented from accumulation of a GFP-tagged kinesin GFP-KCA1; hence, it is called the KCA-depleted zone (KDZ). The KDZ demarcates the cortical division site independent from the mitotic cytoskeleton. Cell divisions in the absence of a KDZ resulted in misplaced cell plates, suggesting that the PPB transmits a signal to the plasma membrane required for correct cell plate guidance and vesicular targeting to the cortical division site.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
334 Leonard St
Brooklyn, NY 11211
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.