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The stem cell niche of the Arabidopsis (Arabidopsis thaliana) primary root apical meristem is composed of the quiescent (or organizing) center surrounded by stem (initial) cells for the different tissues. Initial cells generate a population of transit-amplifying cells that undergo a limited number of cell divisions before elongating and differentiating. It is unclear whether these divisions occur stochastically or in an orderly manner. Using the thymidine analog 5-ethynyl-2'-deoxyuridine to monitor DNA replication of cells of Arabidopsis root meristems, we identified a pattern of two, four, and eight neighboring cells with synchronized replication along the cortical, epidermal, and endodermal cell files, suggested to be daughters, granddaughters, and great-granddaughters of the direct progeny of each stem cell. Markers of mitosis and cytokinesis were not present in the region closest to the transition zone where the cells start to elongate, suggesting that great-granddaughter cells switch synchronously from the mitotic cell cycle to endoreduplication. Mutations in the stem cell niche-expressed ASH1-RELATED3 (ASHR3) gene, encoding a SET-domain protein conferring histone H3 lysine-36 methylation, disrupted this pattern of coordinated DNA replication and cell division and increased the cell division rate in the quiescent center. E2Fa/E2Fb transcription factors controlling the G1-to-S-phase transition regulate ASHR3 expression and bind to the ASHR3 promoter, substantiating a role for ASHR3 in cell division control. The reduced length of the root apical meristem and primary root of the mutant ashr3-1 indicate that synchronization of replication and cell divisions is required for normal root growth and development., (© 2014 American Society of Plant Biologists. All Rights Reserved.)

The giant sequoia and the bristlecone pine trees are capable of living up to several hundreds or even thousands of years. Plants achieve this longevity by regenerating stem cells capable of giving rise to all differentiated cells. Plant stem cells reside in specific niches with high mitotic activity that are known as meristems. Remarkably, at the center of the root stem cell niche (SCN) resides a group of mitotically inactive cells known as the quiescent center (QC). Recent studies suggest that stress-related phytohormones and DNA damage can initiate QC cell division, resulting in the replenishment of stem cells surrounding the QC. We therefore propose that the QC represents a pool of backup cells that serve to replace damaged stem cells, thereby contributing to plant longevity., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Despite being surrounded by highly mitotic active cells, QC cells self-renew at a low proliferation rate. Here, we identified the ERF115 transcription factor as a rate-limiting factor of QC cell division, acting as a transcriptional activator of the phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/C(CCS52A2) ubiquitin ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Together, these two antagonistic mechanisms delimit ERF115 activity, which is called upon when surrounding stem cells are damaged, revealing a cell cycle regulatory mechanism accounting for stem cell niche longevity.

The anaphase-promoting complex/cyclosome (APC/C) is a multisubunit ubiquitin ligase that regulates progression through the cell cycle by marking key cell division proteins for destruction. To ensure correct cell cycle progression, accurate timing of APC/C activity is important, which is obtained through its association with both activating and inhibitory subunits. However, although the APC/C is highly conserved among eukaryotes, no APC/C inhibitors are known in plants. Recently, we have identified ULTRAVIOLET-B-INSENSITIVE4 (UVI4) as a plant-specific component of the APC/C. Here, we demonstrate that UVI4 uses conserved APC/C interaction motifs to counteract the activity of the CELL CYCLE SWITCH52 A1 (CCS52A1) activator subunit, inhibiting the turnover of the A-type cyclin CYCA2;3. UVI4 is expressed in an S phase-dependent fashion, likely through the action of E2F transcription factors. Correspondingly, uvi4 mutant plants failed to accumulate CYCA2;3 during the S phase and prematurely exited the cell cycle, triggering the onset of the endocycle. We conclude that UVI4 regulates the temporal inactivation of APC/C during DNA replication, allowing CYCA2;3 to accumulate above the level required for entering mitosis, and thereby regulates the meristem size and plant growth rate.

This article, published in the Journal of Experimental Botany, explores the activation of dormant stem cell division in response to DNA damage in Arabidopsis thaliana roots. The study found that DNA damage leads to the activation of a signaling module that awakens dormant stem cells to replace those lost through DNA damage. The researchers identified the involvement of the ATM kinase and the SOG1 transcription factor in this process. Additionally, the study revealed that brassinosteroid signaling plays a role in activating stem cell division in response to DNA damage. However, there are still unanswered questions regarding the role of other hormones and the specific triggers for stem cell division. [Extracted from the article]

Quiescent centre (QC) cells represent an integral part of the root stem cell niche. They typically display a low division frequency that has been reported to be controlled by hormone signaling and different regulators, including the ETHYLENE RESPONSE FACTOR 115 (ERF115) transcription factor and D-type cyclins. Here, we applied a three-dimensional (3D) imaging to visualize the Arabidopsis QC cell number, volume and division patterns, including visualization of anticlinal divisions that cannot be deduced from longitudinal 2D imaging. We found that 5-day-old seedlings possess on average eight QC cells which are organized in a monolayered disc. In a period of 7 d, half of the QC cells undergo anticlinal division in a largely invariant space. Ectopic expression of ERF115 and CYCLIN D1;1 (CYCD1;1) promote both anticlinal and periclinal QC cell divisions, the latter resulting in a dual-layered QC zone holding up to 2-fold more QC cells compared with the wild type. In contrast, application of cytokinin or ethylene results in an increase in the number of periclinal, but a decrease in anticlinal QC divisions, suggesting that they control the orientation of QC cell division. Our data illustrate the power of 3D visualization in revealing unexpected QC characteristics. [ABSTRACT FROM AUTHOR]

Plant roots possess remarkable regenerative potential owing to their ability to replenish damaged or lost stem cells. ETHYLENE RESPONSE FACTOR 115 (ERF115), one of the key molecular elements linked to this potential, plays a predominant role in the activation of regenerative cell divisions. However, the downstream operating molecular machinery driving wound-activated cell division is largely unknown. Here, we biochemically and genetically identified the GRAS-domain transcription factor SCARECROW-LIKE 5 (SCL5) as an interaction partner of ERF115 in Arabidopsis thaliana. Although nonessential under control growth conditions, SCL5 acts redundantly with the related PHYTOCHROME A SIGNAL TRANSDUCTION 1 (PAT1) and SCL21 transcription factors to activate the expression of the DNA-BINDING ONE FINGER 3.4 (DOF3.4) transcription factor gene. DOF3.4 expression is wound-inducible in an ERF115-dependent manner and, in turn, activates D3-type cyclin expression. Accordingly, ectopic DOF3.4 expression drives periclinal cell division, while its downstream D3-type cyclins are essential for the regeneration of a damaged root. Our data highlight the importance and redundant roles of the SCL5, SCL21, and PAT1 transcription factors in wound-activated regeneration processes and pinpoint DOF3.4 as a key downstream element driving regenerative cell division. [ABSTRACT FROM AUTHOR]