植物中XRN家族的研究进展

XRN家族是一类5′-3′核酸外切酶家族,主要参与rRNA的成熟加工以及特异mRNA的降解过程,在动物、植物以及微生物的生长发育过程中起着重要的作用.对XRN家族在植物生长发育过程中的功能进行了综述,XRN家族在植物中主要参与rRNA加工过程、miRNA途径、外源mRNA降解过程以及乙烯信号通路.     

真核生物细胞中无终止密码mRNA的降解

2002年,Frischmeyer和Hoof等人发现真核生物细胞中具有一种新的mRNA监视机制——无终止密码mRNA降解途径,与正常mRNA和无义mRNA降解途径不同,无终止密码mRNA是在外切酶体介导作用下快速脱腺苷并进行3’→5’方向的水解。本对无终止密码mRNA降解途径的研究现状做一简要介绍。     

植物氮代谢硝酸还原酶水平调控机制的研究进展

氮代谢是植株体内最基本的物质代谢之一,硝酸还原酶是植物氮代谢的关键酶。主要对植物氮代谢在硝酸还原酶水平上调控的研究新进展,尤其是其合成／降解及活性调控机制进行了较为系统的综述。硝酸还原酶合成的调控主要发生在转录水平和翻译水平上,硝酸还原酶降解的调控主要发生在翻译后水平上,同时NO3^-及光在硝酸还原酶转录水平调控上的作用重大,硝酸还原酶编码基因转录的mRNA的稳定性强弱影响植物的氮代谢,而影响mRNA稳定性的因素很多,机理复杂;磷酸化／去磷酸化在硝酸还原酶活性调控中占举足轻重的地位,研究也比较深入。钝化蛋白也能够影响硝酸还原酶活性,许多小分子物质对硝酸还原酶活性有影响。     

细菌mRNA的降解机制

在细菌中,mRNA降解具有重要的意义,它不仅可以再循环核苷酸,而且还可以根据生长条件的变化调控基因表达.细菌mRNA的降解机制可以分为3种：① mRNA的一般降解途径|② mRNA的质量控制途径|③ 小RNA介导的降解途径. 这些途径有些与真核生物的mRNA降解途径存在很大差异,有些在真核生物中消失了. 另外,mRNA降解途径还可以直接调控细菌致病因子的表达,这使得细菌mRNA的降解途径很有希望成为药物研发的新靶标,或疫苗制备的新平台,以应对越来越严重的细菌耐药性问题.本文综述了细菌mRNA的降解机制,并对其应用前景进行了展望.     

植物逆境胁迫相关miRNA研究进展

MicroRNAs(mi RNAs)是一类内源性小分子的非编码RNA,它通过对其靶基因mRNA的降解或抑制翻译来调控基因表达,进而参与调控植物相关生理活动。在逆境胁迫下,植物中的一些miRNA通过迅速表达并作用于某些与逆境相关的基因,以启动植物的某些抗逆信号系统,进而提高植物对不良环境的适应能力。就miRNA的产生、作用方式、研究方法及其在植物在逆境胁迫中的抗逆作用机制研究进行了综述,并对植物miRNA的研究发展趋势进行了展望。     

miR172-AP2模块调控植物生长发育及逆境响应的研究进展

MicroRNA (miRNA)是一类具有调控能力的非编码小分子RNA, 通过与靶基因mRNA特异或非特异性结合, 诱导靶基因mRNA降解或抑制其翻译, 从而调控植物的生长发育。其中, miR172的靶基因AP2所编码的转录因子为植物所特有, miR172在转录后或翻译水平对AP2进行表达调控, 进而调控植物的花发育、时序转换、小穗形态、块茎和果实发育、结瘤(豆科)以及逆境响应等过程。该文综述了近年来miR172-AP2模块在植物生长发育调控方面的最新研究进展。     

miR172-AP2模块调控植物生长发育及逆境响应的研究进展

MicroRNA(miRNA)是一类具有调控能力的非编码小分子RNA,通过与靶基因mRNA特异或非特异性结合,诱导靶基因mRNA降解或抑制其翻译,从而调控植物的生长发育。其中,miR172的靶基因AP2所编码的转录因子为植物所特有,miR172在转录后或翻译水平对AP2进行表达调控,进而调控植物的花发育、时序转换、小穗形态、块茎和果实发育、结瘤(豆科)以及逆境响应等过程。该文综述了近年来miR172-AP2模块在植物生长发育调控方面的最新研究进展。     

真核生物mRNA降解途径

mRNA降解在真核生物的基因表达调控中发挥重要作用.目前,已经鉴定了多种参与mRNA降解 的酶和复合物,并发现细胞质处理小体可能是降解mRNA的主要位点.本文着重总结了正常和 异常mRNA降解的主要途径以及各途径相关因子和酶的功能,并讨论了细胞质处理小体在mR NA降解过程中的作用.最后对该领域今后的研究重点和方向作了探讨.     

真核细胞中mRNA降解机制研究进展

真核细胞中mRNA的半寿期差异明显，mRNA的降解是基因表达过程中一个重要的步骤，现已肯定在真核细胞中至少存在3种mRNA降解方式，即依赖于脱腺苷酸的降解，无义密码介导的mRNA的降解和核酸内切酶的水解。其中依赖于脱腺苷酸的降解是细胞内大部分mRNA降解的主要途径。另外，mRNA的稳定性还受多种因素影响，现已发现许多影响mRNA稳定性的“顺式因子”和“反式因子”。此外，mRNA降解可能与某些疾病的发生有关。     

RNA deadenylation and decay in plants

In eukaryotic cells, RNA levels are tightly regulated in a spatio-temporal manner to maintain the protein levels necessary for cell growth, differentiation and division. To cope with developmental and rapid environmental changes, RNAs that are no longer required by the cell undergo degradation via the mRNA decay process. A number of players involved in RNA degradation pathways have been identified for the last two decades. A wealth of information about the process of mRNA deadenylation and decay in yeast and other model organisms is currently available; however, very limited information is available in plants, including Arabidopsis. Nevertheless, the efforts of various plant research groups are continuously extending our understanding of this complicated process. Here, we summarize our current knowledge of RNA decay in yeast and compare this information with the progress from Arabidopsis. This review will especially focus on the structure and function of the deadenylation complex, 5′ to 3′ exoribonuclease (XRN)-mediated decay pathways and the exosome-mediated 3′ to 5′ decay pathway in plants.     

Upf1 stimulates degradation of the product derived from aberrant messenger RNA containing a specific nonsense mutation by the proteasome

Aberrant messenger RNAs containing a premature termination codon (PTC) are eliminated by the nonsense‐mediated mRNA decay (NMD) pathway. Here, we show that a crucial NMD factor, up frameshift 1 protein (Upf1), is required for rapid proteasome‐mediated degradation of an aberrant protein (PTC product) derived from a PTC‐containing mRNA. Western blot and pulse–chase analyses revealed that Upf1 stimulates the degradation of specific PTC products by the proteasome. Moreover, the Upf1‐dependent, proteasome‐mediated degradation of the PTC product was also stimulated by mRNAs harbouring a faux 3′ untranslated region (3′‐UTR). These results indicate that protein stability might be regulated by an aberrant mRNA 3′‐UTR.     

p38 Mitogen-activated protein kinase stabilizes mRNAs that contain cyclooxygenase-2 and tumor necrosis factor AU-rich elements by inhibiting deadenylation

AU-rich elements (AREs) in 3'-untranslated regions of mRNAs confer instability. They target mRNAs for rapid deadenylation and degradation and may enhance decapping. The p38 MAPK pathway stabilizes many otherwise unstable ARE-containing mRNAs encoding proteins involved in inflammation; however, the mRNA decay step(s) regulated by the signaling pathway are unknown. To investigate whether it regulates deadenylation or the decay of the mRNA body, we used a tetracycline-regulated beta-globin mRNA reporter system to transcribe pulses of mRNA of uniform length. We measured on Northern gels the migration of reporter mRNAs isolated from cells transfected only with reporter plasmid or co-transfected with an active mutant of MAPK kinase-6, and treated either with or without the p38 MAPK inhibitor SB 203580. Differences in migration were shown by RNase H mapping with oligo(dT) to be due to poly(A) shortening. Insertion of an ARE into the beta-globin reporter mRNA promoted rapid deadenylation and decay of hypo-adenylated reporter mRNA. p38 MAPK activation inhibited the deadenylation of reporter mRNAs containing either the cyclooxygenase-2 or tumor necrosis factor AREs. The regulation of deadenylation by p38 MAPK was found to be specific because deadenylation of the beta-globin reporter mRNA either lacking an ARE or containing the c-Myc 3'-untranslated region (which is not p38 MAPK-responsive) was unaffected by p38 MAPK. It was concluded that the p38 MAPK pathway predominantly regulates deadenylation, rather than decay of the mRNA body, and this provides an explanation for why p38 MAPK regulates mRNA stability in some situations and translation in others.     

Identification of HuR as a protein implicated in AUUUA-mediated mRNA decay.

Expression of many proto-oncogenes, cytokines and lymphokines is regulated by targeting their messenger RNAs for rapid degradation. Essential signals for this control are AU-rich elements (AREs) in the 3' untranslated region (UTR) of these messages. The ARE is loosely defined as the five-nucleotide sequence AUUUA embedded in a uracil-rich region. A transacting factor, presumably a protein, binds the ARE and initiates recognition by the destabilization machinery. Numerous candidate ARE-binding proteins have been proposed. We show that a 32 kDa protein in HeLa nuclear extracts characterized previously has RNA-binding specificity that correlates with the activity of an ARE in directing mRNA decay. Purification and subsequent analyses demonstrate that this 32 kDa protein is identical to a recently identified member of the Elav-like gene family (ELG) called HuR. The in vitro binding selectivity of HuR is indicative of an ARE sequence's ability to destabilize a mRNA in vivo, suggesting a critical role for HuR in the regulation of mRNA degradation.