scholarly journals Transcriptional control of ROS homeostasis by KUODA1 regulates cell expansion during leaf development

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Dandan Lu ◽  
Ting Wang ◽  
Staffan Persson ◽  
Bernd Mueller-Roeber ◽  
Jos H.M. Schippers
2007 ◽  
Vol 144 (2) ◽  
pp. 988-999 ◽  
Author(s):  
Ali Ferjani ◽  
Gorou Horiguchi ◽  
Satoshi Yano ◽  
Hirokazu Tsukaya

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 437
Author(s):  
Charlotte Scholtes ◽  
Vincent Giguère

Reactive oxygen species (ROS) such as superoxide anion (O2•−) and hydrogen peroxide (H2O2) are generated endogenously by processes such as mitochondrial oxidative phosphorylation, or they may arise from exogenous sources like bacterial invasion. ROS can be beneficial (oxidative eustress) as signaling molecules but also harmful (oxidative distress) to cells when ROS levels become unregulated in response to physiological, pathological or pharmacological insults. Indeed, abnormal ROS levels have been shown to contribute to the etiology of a wide variety of diseases. Transcriptional control of metabolic genes is a crucial mechanism to coordinate ROS homeostasis. Therefore, a better understanding of how ROS metabolism is regulated by specific transcription factors can contribute to uncovering new therapeutic strategies. A large body of work has positioned the estrogen-related receptors (ERRs), transcription factors belonging to the nuclear receptor superfamily, as not only master regulators of cellular energy metabolism but, most recently, of ROS metabolism. Herein, we will review the role played by the ERRs as transcriptional regulators of ROS generation and antioxidant mechanisms and also as ROS sensors. We will assess how the control of ROS homeostasis by the ERRs can be linked to physiology and disease and the possible contribution of manipulating ERR activity in redox medicine.


2020 ◽  
Vol 61 (6) ◽  
pp. 1181-1190
Author(s):  
Mamoru Nozaki ◽  
Kensuke Kawade ◽  
Gorou Horiguchi ◽  
Hirokazu Tsukaya

Abstract Leaves are formed by coordinated growth of tissue layers driven by cell proliferation and expansion. Compensation, in which a defect in cell proliferation induces compensated cell enlargement (CCE), plays an important role in cell-size determination during leaf development. We previously reported that CCE triggered by the an3 mutation is observed in epidermal and subepidermal layers in Arabidopsis thaliana (Arabidopsis) leaves. Interestingly, CCE is induced in a non-cell autonomous manner between subepidermal cells. However, whether CCE in the subepidermis affects cell size in the adjacent epidermis is still unclear. We induced layer-specific expression of AN3 in an3 leaves and found that CCE in the subepidermis had little impact on cell-size determination in the epidermis, and vice versa, suggesting that CCE is induced in a tissue-autonomous manner. Examination of the epidermis in an3 leaves having AN3-positive and -negative sectors generated by Cre/loxP revealed that, in contrast to the subepidermis, CCE occurred exclusively in AN3-negative epidermal cells, indicating a cell autonomous action of an3-mediated compensation in the epidermis. These results clarified that the epidermal and subepidermal tissue layers have different cell autonomies in CCE. In addition, quantification of cell-expansion kinetics in epidermal and subepidermal tissues of the an3 showed that the tissues exhibited a similar temporal profile to reach a peak cell-expansion rate as compared to wild type. This might be one feature representing that the two tissue layers retain their growth coordination even in the presence of CCE.


2020 ◽  
Author(s):  
Yaxin Gong ◽  
Han Yue ◽  
Yu Xiang ◽  
Guanghui Yu

AbstractTo investigate the molecular mechanism underlying increasing leaf area in γ-Aminobutyric acid (GABA) biosynthetic mutants, the first pair of true leaves of GABA biosynthetic mutants was measured. The results showed that the leaf blade area in GABA biosynthetic mutants was larger than that of the wild type to different extents, and the area of the leaf epidermal cells in mutants was larger than that of the wild type. DNA polyploid analysis showed that polyploid cells in GABA biosynthetic mutants were appearing earlier and more abundant than in the wild type. To check the correlation between cell size and endoreplication, the expression of factors involving endocycles, including D-type cyclin gene (CYCD3;1, CYCD3;2, CYCD3;3, and CYCD4;1) and kinase CKDA;1, were analysed by qRT-PCR. The results showed that CKDA;1 in GABA biosynthetic mutants was downregulated, and four types of CYCDs showed different expression patterns in different GABA biosynthetic mutants. Inconsistent with this result, for CCS52A (CELL CYCLE SWITCH 52A) (controlling the endocycle entry) in gad2 and gad1/gad2 mutants, the expression of CCS52A2 was significantly higher than that in the wild type. The expression of SIM (SIAMESE) and SMR (SIAMESE-RELATED), which inhibit kinase activity, were also upregulated compared with the control. To further study the possible potential relationship between GABA metabolism and endoreplication, we analysed the reactive oxygen species (ROS) levels in guard cells using ROS fluorescent probes. ROS levels were significantly higher in GABA biosynthetic mutants than the control. All results indicated that cyclin, the cyclin-dependent kinase, and its inhibitory protein were coordinated to participate in endoreplication control at the transcription level in the leaves of GABA biosynthetic mutant Arabidopsis.Contribution to the field statementγ-Aminobutyric acid (GABA) metabolic pathway plays a dual role in plant development. This research investigated the perturbation of GABA biosynthesis on Arabidopsis leave endoreplication for the first time. In the GABA biosynthetic mutants, many genes, participating in cell division regulation, are coordinately transcriptionally expressed to trigger the onset and maintenance of endoreplication, and this led to the cell expansion and the increase leaf blade area. However, this initiation of endoreplication links with the decrease of endogenous GABA level and the increase Reactive oxygen species (ROS). This may be a compensation mechanism to adapt to abnormal GABA level in plant leaf development. Present evidence provided hypothesized that the normal GABA level in plant leaf development plays a brake to inhibit the immature cell expansion and differentiation, and this negative regulation functions a guarantee mechanism to watchdog the normal leaf development. In all, this contribution provides an updated perspective on the role of GABA in plant development.


Genes ◽  
2019 ◽  
Vol 10 (9) ◽  
pp. 644 ◽  
Author(s):  
Yoon-Sun Hur ◽  
Jiyoung Kim ◽  
Sunghan Kim ◽  
Ora Son ◽  
Woo-Young Kim ◽  
...  

Leaves grow by distinct phases controlled by gene regulatory networks including many transcription factors. Arabidopsis thaliana homeobox 12 (ATHB12) promotes leaf growth especially during the cell expansion phase. In this study, we identify TCP13, a member of the TCP transcription factor family, as an upstream inhibitor of ATHB12. Yeast one-hybrid screening using a 1.2-kb upstream region of ATHB12 resulted in the isolation of TCP13 as well as other transcription factors. Transgenic plants constitutively expressing TCP13 displays a significant reduction in leaf cell size especially during the cell expansion period, while repression of TCP13 and its paralogs (TCP5 and TCP17) result in enlarged leaf cells, indicating that TCP13 and its paralogs inhibit leaf development, mainly at the cell expansion phase. Its expression pattern during leaf expansion phase is opposite to ATHB12 expression. Consistently, the expression of ATHB12 and its downstream genes decreases when TCP13 was overexpressed, and increases when the expression of TCP13 and its paralogs is repressed. In chromatin immunoprecipitation assays using TCP13-GFP plants, a fragment of the ATHB12 upstream region that contains the consensus sequence for TCP binding is strongly enriched. Taken together, these findings indicate that TCP13 and its paralogs inhibit leaf growth by repressing ATHB12 expression.


2008 ◽  
Vol 319 (2) ◽  
pp. 610
Author(s):  
Daniel Hill ◽  
Xingyuan Ling ◽  
Anding Luo ◽  
Mike Tamkun ◽  
Anne Sylvester

2019 ◽  
Vol 71 (8) ◽  
pp. 2365-2378 ◽  
Author(s):  
Jasmien Vercruysse ◽  
Alexandra Baekelandt ◽  
Nathalie Gonzalez ◽  
Dirk Inzé

Abstract Leaves are the primary organs for photosynthesis, and as such have a pivotal role for plant growth and development. Leaf development is a multifactorial and dynamic process involving many genes that regulate size, shape, and differentiation. The processes that mainly drive leaf development are cell proliferation and cell expansion, and numerous genes have been identified that, when ectopically expressed or down-regulated, increase cell number and/or cell size during leaf growth. Many of the genes regulating cell proliferation are functionally interconnected and can be grouped into regulatory modules. Here, we review our current understanding of six important gene regulatory modules affecting cell proliferation during Arabidopsis leaf growth: ubiquitin receptor DA1–ENHANCER OF DA1 (EOD1), GROWTH REGULATING FACTOR (GRF)–GRF-INTERACTING FACTOR (GIF), SWITCH/SUCROSE NON-FERMENTING (SWI/SNF), gibberellin (GA)–DELLA, KLU, and PEAPOD (PPD). Furthermore, we discuss how post-mitotic cell expansion and these six modules regulating cell proliferation make up the final leaf size.


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