Mutation of<i>Arabidopsis BARD1</i>Causes Meristem Defects by Failing to Confine<i>WUSCHEL</i>Expression to the Organizing Center

Han, Pei; Li, Qing; Zhu, Yu-Xian

doi:10.1105/tpc.108.058867

Cited by 63 publications

(70 citation statements)

References 47 publications

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“…A mutation in the BRCA1-associated RING domain1 gene caused both a defect in DNA repair and in the maintenance of SAM organization by repressing WUS expression in plants (Reidt et al, 2006;Han et al, 2008). In a previous study, double-knockdown lines of the cyclin-dependent kinases CDKB2;1 and CDKB2;2 showed abnormal SAMs and phyllotaxis, suggesting a close link between cell cycle progression and the regulation of meristem organization in plants (Andersen et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

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A DNA2 Homolog Is Required for DNA Damage Repair, Cell Cycle Regulation, and Meristem Maintenance in Plants

2016

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Plant meristem cells divide and differentiate in a spatially and temporally regulated manner, ultimately giving rise to organs. In this study, we isolated the Arabidopsis jing he sheng 1 (jhs1) mutant, which exhibited retarded growth, an abnormal pattern of meristem cell division and differentiation, and morphological defects such as fasciation, an irregular arrangement of siliques, and short roots. We identified JHS1 as a homolog of human and yeast DNA Replication Helicase/Nuclease2, which is known to be involved in DNA replication and damage repair. JHS1 is strongly expressed in the meristem of Arabidopsis. The jhs1 mutant was sensitive to DNA damage stress and had an increased DNA damage response, including increased expression of genes involved in DNA damage repair and cell cycle regulation, and a higher frequency of homologous recombination. In the meristem of the mutant plants, cell cycle progression was delayed at the G2 or late S phase and genes essential for meristem maintenance were misregulated. These results suggest that JHS1 plays an important role in DNA replication and damage repair, meristem maintenance, and development in plants.

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Section: Discussionmentioning

confidence: 99%

“…10). It has been suggested that overexpression of WUS and STM may disorganize the SAM (Han et al, 2008) and result in fasciation. Thus, it is likely that DNA damage causes fasciation by promoting the overexpression of WUS and STM.…”

Section: Discussionmentioning

confidence: 99%

A DNA2 Homolog Is Required for DNA Damage Repair, Cell Cycle Regulation, and Meristem Maintenance in Plants

2016

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“…When low RBR levels persisted, however, meristem activity could not recover and WUS expression was reduced again to normal levels, although CLV3 expression remained low (Figure 3). Thus, WUS expression might be repressed by a CLV-independent mechanism, such as BREAST CANCER ASSOCIATED RING1 (BARD1) (Han et al, 2008), which is strongly upregulated in induced RBRi seedlings (Figure 3). A detailed temporal and spatial analysis of WUS and other genes involved in SAM organization will be required to better understand their functions during RBR downregulation.…”

Section: Rbr Homeostasis Is Critical For Meristem Integrity and Functionmentioning

confidence: 99%

“…Five days after germination on b-estradiol, CYCB1;1 was upregulated in the SAM, as we observed in leaves (see Figure 5). BARD1 (reported to limit WUS expression; Han et al, 2008), is strongly upregulated 5 d after induction. The error bars represent the SE from two biological replicas and two technical replicas.…”

Section: Rbr Regulates Meristemoid Proliferation and Subsequent Stomamentioning

confidence: 99%

ArabidopsisRETINOBLASTOMA-RELATED Is Required for Stem Cell Maintenance, Cell Differentiation, and Lateral Organ Production

et al. 2010

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Several genes involved in the regulation of postembryonic organ initiation and growth have been identified. However, it remains largely unclear how developmental cues connect to the cell cycle. RETINOBLASTOMA RELATED (RBR) is a plant homolog of the tumor suppressor Retinoblastoma (pRb), which is a key regulator of the cell cycle. Using inducible RNA interference (RNAi) against Arabidopsis thaliana RBR (RBRi), we reduced RBR expression levels at different stages of plant development. Conditional reduction or loss of RBR function disrupted cell division patterns, promoted context-dependent cell proliferation, and negatively influenced establishment of cell differentiation. Several lineages of toti-and pluripotent cells, including shoot apical meristem stem cells, meristemoid mother cells, and procambial cells, failed to produce appropriately differentiated cells. Meristem activity was altered, leading to a disruption of the CLAVATA-WUSCHEL feedback loop and inhibition of lateral organ formation. Release of RBR from RNAi downregulation restored meristem activity. Gene profiling analyses soon after RBRi induction revealed that a change in RBR homeostasis is perceived as a stress, even before genes regulated by RBR-E2F become deregulated. The results establish RBR as a key cell cycle regulator required for coordination of cell division, differentiation, and cell homeostasis. INTRODUCTIONRetinoblastoma (RB) was the first tumor suppressor gene identified in animals (Friend et al., 1986) and later was associated with cell cycle regulation, thus establishing pRb as a key regulator of cell proliferation. In animals, three members of the RB family of proteins (pRb, p107, and p130), also referred to as pocket proteins (Mulligan and Jacks, 1998), negatively regulate the G1-to-S phase transition during the cell cycle. It is now widely accepted that mitogenic signals activate several cyclin-dependent kinase (CDK)-cyclin complexes during progression through G1 to phosphorylate pRb, thereby releasing it from interactions with E2F/DP transcription factor complexes to facilitate S-phase entry (Weinberg, 1995). Subsequently, pRb was also found to regulate tissue-specific transcription factors that regulate cell differentiation, such as MyoD, which activates muscle-specific genes (De Falco et al., 2006). pRb also regulates germ cell proliferation, differentiation, and survival (Toppari et al., 2003) and is required for osteoblast, keratinocyte, and macrophage differentiation (Nead et al., 1998;Liu et al., 1999;Thomas et al., 2003). Together with the tumor suppressor p53, pRb regulates adipocyte differentiation and function (Hallenborg et al., 2009). The requirement for RB in cell differentiation therefore extends beyond regulation of cell cycle entry. For example, the loss of RB function in cardioblasts affects cell differentiation by modulating the activity of cardiogenic factors (Papadimou et al., 2005).RB-related genes, termed RETINOBLASTOMA-RELATED (RBR; Ach et al., 1997), are also found in monocots (Grafi et al., 1996;Xie et al...

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“…DPa interacts with the E2Fa transcription factor to form a complex that stimulates the expression of S phase-specific genes, leading to cell division and a delay of cell differentiation (De Veylder et al, 2002). BARD1 has been reported to control SAM organization and maintenance by restricting WUSCHEL (WUS) expression to the organizing center (Han et al, 2008). WUS encodes a homeodomain Figure 6.…”

Section: Ebe-triggered Changes In Gene Expressionmentioning

confidence: 99%

EBE, an AP2/ERF Transcription Factor Highly Expressed in Proliferating Cells, Affects Shoot Architecture in Arabidopsis

et al. 2013

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We report about ERF BUD ENHANCER (EBE; At5g61890), a transcription factor that affects cell proliferation as well as axillary bud outgrowth and shoot branching in Arabidopsis (Arabidopsis thaliana). EBE encodes a member of the APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) transcription factor superfamily; the gene is strongly expressed in proliferating cells and is rapidly and transiently up-regulated in axillary meristems upon main stem decapitation. Overexpression of EBE promotes cell proliferation in growing calli, while the opposite is observed in EBE-RNAi lines. EBE overexpression also stimulates axillary bud formation and outgrowth, while repressing it results in inhibition of bud growth. Global transcriptome analysis of estradiolinducible EBE overexpression lines revealed 48 EBE early-responsive genes, of which 14 were up-regulated and 34 were downregulated. EBE activates several genes involved in cell cycle regulation and dormancy breaking, including D-type cyclin CYCD3;3, transcription regulator DPa, and BRCA1-ASSOCIATED RING DOMAIN1. Among the down-regulated genes were DORMANCY-ASSOCIATED PROTEIN1 (AtDRM1), AtDRM1 homolog, MEDIATOR OF ABA-REGULATED DORMANCY1, and ZINC FINGER HOMEODOMAIN5. Our data indicate that the effect of EBE on shoot branching likely results from an activation of genes involved in cell cycle regulation and dormancy breaking.

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Mutation ofArabidopsis BARD1Causes Meristem Defects by Failing to ConfineWUSCHELExpression to the Organizing Center

Cited by 63 publications

References 47 publications

A DNA2 Homolog Is Required for DNA Damage Repair, Cell Cycle Regulation, and Meristem Maintenance in Plants

A DNA2 Homolog Is Required for DNA Damage Repair, Cell Cycle Regulation, and Meristem Maintenance in Plants

ArabidopsisRETINOBLASTOMA-RELATED Is Required for Stem Cell Maintenance, Cell Differentiation, and Lateral Organ Production

EBE, an AP2/ERF Transcription Factor Highly Expressed in Proliferating Cells, Affects Shoot Architecture in Arabidopsis

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