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2月12植物updates: SRT1or2介導(dǎo)乙烯轉(zhuǎn)錄抑制;擬南芥JMJ14-H3K4me3復(fù)合物;HY5轉(zhuǎn)錄因子調(diào)控測(cè)根機(jī)制

 PaperRSS 2020-01-14

Histone(組蛋白) Deacetylases SRT1 and SRT2 Interact with ENAP1 to Mediate Ethylene-Induced Transcriptional Repression

Fan ZhangLikai WangEun Esther KoKevin ShaoHong Qiao

Published January 2018. DOI: http://dx./10.1105/tpc.17.00671

來(lái)自:美國(guó)德克薩斯大學(xué)奧斯汀分校

Abstract

Ethylene(乙烯) plays pleiotropic(多效性的) roles in plant growth, plant development, and stress responses. Although the effects of ethylene on plants are well documented, little is known about molecular-level events that result in transcriptional repression(抑制) during the ethylene response. In this study, we found that two histone(組蛋白) deacetylases(脫乙酰酶), SRT1 and SRT2, interact with ENAP1, which associates with EIN2 in the nucleus(核). Genetic and transcriptome analyses revealed that SRT1 and SRT2 are required for negative regulation of certain ethylene-responsive genes. The acetylation(乙?;饔? of HISTONE3 at K9 (H3K9Ac) is specifically regulated by SRT1 and SRT2 in ethylene-repressed genes. In addition, the srt1 srt2 double mutation in Arabidopsis thaliana suppresses both the ENAP1ox and the EIN3ox constitutive(基本的) ethylene response phenotypes(表型), and the ethylene-induced transcriptional repression observed in EIN3ox plants is derepressed(去阻遏) in the EIN3ox/srt1 srt2 mutant(突變體). SRT2 and ENAP1 both bind to promoter regions of genes negatively regulated by ethylene(乙烯), reducing H3K9Ac levels and resulting in transcriptional repression(抑制). This work establishes a mechanism by which histone(組蛋白) deacetylases(脫乙酰酶) SRT1 and SRT2 interact with ENAP1 to mediate transcriptional repression by regulating the levels of H3K9 acetylation(乙酰化作用) in the ethylene signaling.

乙烯在植物生長(zhǎng),植物發(fā)育和脅迫反應(yīng)中起著多種作用。盡管乙烯對(duì)植物的影響已有文獻(xiàn)報(bào)道,但對(duì)乙烯響應(yīng)過(guò)程中導(dǎo)致轉(zhuǎn)錄抑制的分子水平事件知之甚少。在本研究中,我們發(fā)現(xiàn)兩個(gè)組蛋白脫乙酰酶SRT1和SRT2與ENAP1相互作用,ENAP1與核內(nèi)的EIN2相關(guān)聯(lián)。遺傳和轉(zhuǎn)錄組分析揭示SRT1和SRT2是負(fù)調(diào)控某些乙烯反應(yīng)基因所必需的。 HISTONE3在K9(H3K9Ac)處的乙?;芤蚁┮种苹蛑械腟RT1和SRT2特異性調(diào)節(jié)。此外,擬南芥中的srt1 srt2雙重突變抑制ENAP1ox和EIN3ox組成型乙烯響應(yīng)表型,并且在EIN3ox植物中觀察到的乙烯誘導(dǎo)的轉(zhuǎn)錄阻遏在EIN3ox / srt1 srt2突變體中被去阻遏。 SRT2和ENAP1都與受乙烯負(fù)調(diào)控的基因的啟動(dòng)子區(qū)域結(jié)合,降低H3K9Ac水平并導(dǎo)致轉(zhuǎn)錄抑制。這項(xiàng)工作建立了一個(gè)機(jī)制,其中組蛋白脫乙酰酶SRT1和SRT2與ENAP1相互作用,通過(guò)調(diào)節(jié)乙烯信號(hào)傳導(dǎo)中H3K9乙?;浇閷?dǎo)轉(zhuǎn)錄抑制。

ENAP1 Interacts with SRT1 and SRT2 in Vitro and in Vivo.

srt1 srt2 Rescues the EIN3ox Phenotype. 

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2Plant cell| 通過(guò)HY5轉(zhuǎn)錄因子調(diào)控開(kāi)放閱讀中的遠(yuǎn)紅光檢測(cè)調(diào)節(jié)側(cè)根發(fā)育

Far-Red Light Detection in the Shoot Regulates Lateral Root Development through the HY5 Transcription Factor

來(lái)自:荷蘭烏特勒支大學(xué)生物系

    Abstract

Plants in dense vegetation(植被) compete for resources and detect competitors through reflection of far-red (FR) light from surrounding plants. This reflection causes a reduced red (R):FR ratio, which is sensed through phytochromes(光敏色素). Low R:FR induces shade avoidance(逃避) responses of the shoot and also changes the root system architecture, although this has received little attention so far. Here, we investigate the molecular mechanisms through which light detection in the shoot regulates root development in Arabidopsis thaliana. We do so using a combination of microscopy(顯微鏡檢查), gene expression, and mutant(突變體) study approaches in a setup that allows root imaging without exposing the roots to light treatment. We show that low R:FR perception in the shoot decreases the lateral root (LR) density by inhibiting(抑制) LR emergence(出現(xiàn)). This decrease in LR emergence upon shoot FR enrichment(豐富) is regulated by phytochrome-dependent accumulation of the transcription factor ELONGATED HYPOCOTYL5 (HY5) in the LR primordia(原基). HY5 regulates LR emergence by decreasing the plasma membrane abundance of PIN-FORMED3 and LIKE-AUX1 3 auxin(植物生長(zhǎng)素) transporters. Accordingly, FR enrichment reduces the auxin signal in the overlaying cortex(皮質(zhì)) cells, and this reduces LR outgrowth. This shoot-to-root communication can help plants coordinate resource partitioning under competition for light in high density fields.

Supplemental FR Experienced by the Shoot Leads to Reduced Lateral and Primary Root Growth.

    Enhanced Availability of HY5 under FR Enrichment Inhibits Lateral Root Emergence.

密集植物中的植物競(jìng)爭(zhēng)資源,通過(guò)反射來(lái)自周?chē)参锏倪h(yuǎn)紅光(FR)來(lái)檢測(cè)競(jìng)爭(zhēng)者。這種反射導(dǎo)致通過(guò)光敏色素感測(cè)到的紅(R):FR比率降低。低R:FR誘導(dǎo)枝條的遮蔭避免響應(yīng),并且也改變了根系統(tǒng)結(jié)構(gòu),盡管迄今為止這已經(jīng)不太受關(guān)注。在這里,我們調(diào)查的分子機(jī)制,通過(guò)其中光檢測(cè)調(diào)節(jié)擬南芥根發(fā)育。我們這樣做是在顯微鏡,基因表達(dá)和突變研究方法的結(jié)合下進(jìn)行的,這種方法允許根成像,而不需要將根暴露于光照處理。我們表明,在射擊低R:FR感知通過(guò)抑制LR的出現(xiàn)減少側(cè)根(LR)密度。這種LR出現(xiàn)在枝條FR富集時(shí)的減少受到LR原基中轉(zhuǎn)錄因子ELONGATED HYPOCOTYL5(HY5)的光敏色素依賴性積累的調(diào)節(jié)。 HY5通過(guò)降低PIN-FORMED3和LIKE-AUX1 3生長(zhǎng)素轉(zhuǎn)運(yùn)蛋白的質(zhì)膜豐度來(lái)調(diào)節(jié)LR的出現(xiàn)。因此,富集FR減少了重疊的皮層細(xì)胞中的生長(zhǎng)素信號(hào),并且這降低了LR長(zhǎng)出。這種基于對(duì)話的交流可以幫助植物在高密度領(lǐng)域的光照競(jìng)爭(zhēng)下協(xié)調(diào)資源分配。

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3Plant  cell|擬南芥JMJ14-H3K4me3復(fù)合物的結(jié)構(gòu)讓我們對(duì)KDM5亞家族組蛋白去甲基化酶的底物特異性有深度了解。

Structure of the Arabidopsis JMJ14-H3K4me3 Complex Provides Insight into the Substrate Specificity of KDM5 Subfamily Histone Demethylases

Zhenlin YangQi QiuWei ChenBei JiaXiaomei ChenHongmiao HuKaixuan HeXian DengSisi LiW. Andy TaoXiaofeng CaoJiamu Du

來(lái)源:

1Jiamu Du

中科院上海植物逆境生物學(xué)研究中心杜嘉木研究組招聘博士后

National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Center for Plant Stress Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201602, China

2 Xiaofeng Cao

曹曉風(fēng)院士、中國(guó)科學(xué)院遺傳與發(fā)育研究所研究員

University of Chinese Academy of Sciences, Beijing 100049, ChinaState Key Laboratory of Plant Genomics and National Center for Plant Gene Research, CAS Center for Excellence in Molecular Plant Sciences, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China

在染色質(zhì)中,組蛋白甲基化影響動(dòng)物和植物中多個(gè)過(guò)程的表觀遺傳調(diào)節(jié),并受組蛋白甲基轉(zhuǎn)移酶和組蛋白去甲基化酶的活性調(diào)節(jié)。含有jumonji結(jié)構(gòu)域的組蛋白去甲基化酶具有不同的功能,可分為幾個(gè)亞家族。在人類中,含有jumonji結(jié)構(gòu)域的賴氨酸(K)特異性脫甲基酶5 / Jumonji和ARID結(jié)構(gòu)域蛋白(KDM5 / JARID)亞家族脫甲基酶對(duì)組蛋白3賴氨酸4三甲基化(H3K4me3)是特異性的,并且是癌癥治療的重要藥物靶標(biāo)。在擬南芥中,KDM5 / JARID亞家族H3K4me3脫甲基化酶JUMONJI14(JMJ14)在開(kāi)花,基因沉默和DNA甲基化中起重要作用。在這里,我們報(bào)告了無(wú)基質(zhì)和結(jié)合形式的JMJ14催化結(jié)構(gòu)域的晶體結(jié)構(gòu)。結(jié)構(gòu)顯示jumonji和C5HC2結(jié)構(gòu)域有助于H3R2和H3Q5的特異性識(shí)別以促進(jìn)H3K4me3底物特異性。關(guān)鍵的酸性殘基在植物和動(dòng)物中是保守的,相應(yīng)的突變會(huì)損害JMJ14和人KDM5B的酶活性,表明KDM5亞家族脫甲基酶與植物和動(dòng)物共有的共同底物識(shí)別機(jī)制,并進(jìn)一步說(shuō)明設(shè)計(jì)人類靶向抑制劑的努力KDM5。

    Abstract

In chromatin(核染色質(zhì))histone(組蛋白) methylation(甲基化) affects the epigenetic(后生的)regulation of multiple processes in animals and plants and is modulated(已調(diào)的) by the activities of histone methyltransferases(甲基轉(zhuǎn)移酶) and histone demethylases. The jumonji domain-containing histone demethylases have diverse functions and can be classified into several subfamilies(亞科). In humans, the jumonji domain-containing Lysine(賴氨酸) (K)-Specific Demethylase 5/Jumonji and ARID Domain Protein (KDM5/JARID) subfamily demethylases are specific for histone 3 lysine 4 trimethylation (H3K4me3) and are important drug targets for cancer treatment. In Arabidopsis thaliana, the KDM5/JARID subfamily H3K4me3 demethylase JUMONJI14 (JMJ14) plays important roles in flowering, gene silencing, and DNA methylation. Here, we report the crystal structures of the JMJ14 catalytic domain in both substrate-free and bound forms. The structures reveal that the jumonji and C5HC2 domains contribute to the specific recognition of the H3R2 and H3Q5 to facilitate H3K4me3 substrate specificity(特異性). The critical acidic(酸的) residues are conserved(保存) in plants and animals with the corresponding mutations impairing(損害) the enzyme activity of both JMJ14 and human KDM5B, indicating a common substrate recognition mechanism for KDM5 subfamily demethylases shared by plants and animals and further informing efforts to design targeted inhibitors of human KDM5


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