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An Auxin-Inducible F-Box Protein CEGENDUO Negatively Regulates Auxin-Mediated Lateral Root Formation in Arabidopsis 总被引:4,自引:0,他引:4
Previously, we characterized 92 Arabidopsis genes (AtSFLs) similar to the S-locus F-box genes involved in S-RNase-based self-incompatibility and found that they likely play diverse roles in Arabidopsis. In this study, we investigated the role of one of these genes, CEGENDUO (CEG, AtSFL61), in the lateral root formation. A T-DNA insertion in CEG led to an increased lateral root production, which was complemented by transformation of the wild-type gene. Its downregulation
by RNAi also produced more lateral roots in transformed Arabidopsis plants whereas its overexpression generated less lateral roots compared to wild-type, indicating that CEG acts as a negative
regulator for the lateral root formation. It was found that CEG was expressed abundantly in vascular tissues of the primary root, but not in newly formed lateral root primordia and the
root meristem, and induced by exogenous auxin NAA (α-naphthalene acetic acid). In addition, the ceg mutant was hyposensitive to NAA, IAA (indole-3-acetic acid) and 2,4-D (2,4-dichlorophenoxyacetic acid), as well as the auxin
transport inhibitor TIBA (3,3,5-triiodobenzoic acid), showing that CEG is an auxin-inducible gene. Taken together, our results show that CEG is a novel F-box protein negatively regulating the
auxin-mediated lateral root formation in Arabidopsis.
Electronic supplementary material Electronic supplementary material is available for this article at
and accessible for authorised users. 相似文献
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The RUNX2 Transcription Factor Negatively Regulates SIRT6 Expression to Alter Glucose Metabolism in Breast Cancer Cells 下载免费PDF全文
Moran Choe Jessica L. Brusgard Saranya Chumsri Lekhana Bhandary Xianfeng Frank Zhao Song Lu Olga G. Goloubeva Brian M. Polster Gary M. Fiskum Geoffrey D. Girnun Myoung Sook Kim Antonino Passaniti 《Journal of cellular biochemistry》2015,116(10):2210-2226
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Tadayuki Tsujita Vivian Peirce Liam Baird Yuka Matsuyama Misaki Takaku Shawn V. Walsh Julian L. Griffin Akira Uruno Masayuki Yamamoto John D. Hayes 《Molecular and cellular biology》2014,34(20):3800-3816
Liver-specific Nrf1 (NF-E2-p45-related factor 1) knockout mice develop nonalcoholic steatohepatitis. To identify postnatal mechanisms responsible for this phenotype, we generated an inducible liver-specific Nrf1 knockout mouse line using animals harboring an Nrf1flox allele and a rat CYP1A1-Cre transgene (Nrf1flox/flox::CYP1A1-Cre mice). Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1flox/flox::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 expression. The livers of mice lacking Nrf1 accumulated lipid, and the hepatic fatty acid (FA) composition in such animals differed significantly from that in the Nrf1flox/flox::CYP1A1-Cre control. This change was provoked by upregulation of several FA metabolism genes. Unexpectedly, we also found that the level of glutathione was increased dramatically in livers of Nrf1flox/flox::CYP1A1-Cre+3MC mice. While expression of glutathione biosynthetic enzymes was unchanged, xCT, a component of the cystine/glutamate antiporter system xc−, was significantly upregulated in livers of Nrf1flox/flox::CYP1A1-Cre+3MC mice, suggesting that Nrf1 normally suppresses xCT. Thus, stress-inducible expression of xCT is a two-step process: under homeostatic conditions, Nrf1 effectively suppresses nonspecific transactivation of xCT, but when cells encounter severe oxidative/electrophilic stress, Nrf1 is displaced from an antioxidant response element (ARE) in the gene promoter while Nrf2 is recruited to the ARE. Thus, Nrf1 controls both the FA and the cystine/cysteine content of hepatocytes by participating in an elaborate regulatory network. 相似文献
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谷氧还蛋白(GRX)是一类以CXXC/S基序为活性位点的小分子热稳定蛋白,参与多种谷胱甘肽依赖的氧化还原反应。通过对该家族的GRXC9基因进行克隆、表达、亚细胞定位及功能分析,结果表明,GRXC9基因表达无组织特异性,在拟南芥(Arabidopsis thaliana)的根、茎、叶、花和角果中均能表达,此结果与GUS显色结果基本一致。GRXC9-GFP定位于细胞质和细胞核中,过表达GRXC9的株系叶片明显小于野生型;进一步观察发现,其叶片栅栏细胞明显变小,而细胞总数与野生型差距不大。叶片大小相关基因的表达分析结果表明,过表达株系中AN、LNG1和LNG2的表达量明显下降,说明GRXC9可能通过抑制这些基因的表达从而导致叶片短小。综上所述,GRXC9可能在调控叶片发育方面发挥关键作用。 相似文献
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Chloroplast division is performed by the constriction of envelope membranes at the division site. Although constriction of a ring-like protein complex has been shown to be involved in chloroplast division, it remains unknown how membrane lipids participate in the process. Here, we show that phosphoinositides with unknown function in envelope membranes are involved in the regulation of chloroplast division in Arabidopsis thaliana. PLASTID DIVISION1 (PDV1) and PDV2 proteins interacted specifically with phosphatidylinositol 4-phosphate (PI4P). Inhibition of phosphatidylinositol 4-kinase (PI4K) decreased the level of PI4P in chloroplasts and accelerated chloroplast division. Knockout of PI4Kβ2 expression or downregulation of PI4Kα1 expression resulted in decreased levels of PI4P in chloroplasts and increased chloroplast numbers. PI4Kα1 is the main contributor to PI4P synthesis in chloroplasts, and the effect of PI4K inhibition was largely abolished in the pdv1 mutant. Overexpression of DYNAMIN-RELATED PROTEIN5B (DRP5B), another component of the chloroplast division machinery, which is recruited to chloroplasts by PDV1 and PDV2, enhanced the effect of PI4K inhibition, whereas overexpression of PDV1 and PDV2 had additive effects. The amount of DRP5B that associated with chloroplasts increased upon PI4K inhibition. These findings suggest that PI4P is a regulator of chloroplast division in a PDV1- and DRP5B-dependent manner. 相似文献
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Plants are equipped to recognize invading pathogenic microbes and activate innate immune responses by sensing pathogen-associated molecular patterns (PAMPs). PAMP-triggered immunity (PTI) is critical for plant resistance to potential pathogens. Although the mechanism by which PTI is activated has been intensively studied, exactly how plants prevent unregulated immune responses is less well understood. Here we provide evidence that AHL20, an AT-hook containing DNA-binding protein, negatively regulates PTI. Overexpression of AHL20 as a stable transgene suppressed PAMP-induced NHO1 and FRK1 expression in Arabidopsis plants. Similarly, transient expression of the closely related family members AHL19, AHL15, and AHL27 in protoplasts also blocked PAMP-induced gene expression. The AHL20 overexpression plants displayed greater susceptibility to virulent Pseudomonas syringae bacteria. These results indicate that AHL proteins play an important role in plant immunity. 相似文献
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C McBerry CE Egan R Rani Y Yang D Wu N Boespflug L Boon B Butcher J Mirpuri SP Hogan EY Denkers J Aliberti DR Herbert 《Journal of immunology (Baltimore, Md. : 1950)》2012,189(6):3078-3084
IL-12-mediated type 1 inflammation confers host protection against the parasitic protozoan Toxoplasma gondii. However, production of IFN-γ, another type 1 inflammatory cytokine, also drives lethality from excessive injury to the intestinal epithelium. As mechanisms that restore epithelial barrier function following infection remain poorly understood, this study investigated the role of trefoil factor 2 (TFF2), a well-established regulator of mucosal tissue repair. Paradoxically, TFF2 antagonized IL-12 release from dendritic cells (DCs) and macrophages, which protected TFF2-deficient (TFF2(-/-)) mice from T. gondii pathogenesis. Dysregulated intestinal homeostasis in naive TFF2(-/-) mice correlated with increased IL-12/23p40 levels and enhanced T cell recruitment at baseline. Infected TFF2(-/-) mice displayed low rates of parasite replication and reduced gut immunopathology, whereas wild-type (WT) mice experienced disseminated infection and lethal ileitis. p38 MAPK activation and IL-12p70 production was more robust from TFF2(-/-)CD8(+) DC compared with WT CD8(+) DC and treatment of WT DC with rTFF2 suppressed TLR-induced IL-12/23p40 production. Neutralization of IFN-γ and IL-12 in TFF2(-/-) animals abrogated resistance shown by enhanced parasite replication and infection-induced morbidity. Hence, TFF2 regulated intestinal barrier function and type 1 cytokine release from myeloid phagocytes, which dictated the outcome of oral T. gondii infection in mice. 相似文献