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两个过量产生乙烯的拟南芥突变体在1-氨基环丙烷-1-羧酸合酶的转录后调控方面受到影响。

Two Arabidopsis mutants that overproduce ethylene are affected in the posttranscriptional regulation of 1-aminocyclopropane-1-carboxylic acid synthase.

作者信息

Woeste K E, Ye C, Kieber J J

机构信息

Department of Biological Sciences, Laboratory for Molecular Biology, University of Illinois at Chicago, Chicago, Illinois 60607, USA.

出版信息

Plant Physiol. 1999 Feb;119(2):521-30. doi: 10.1104/pp.119.2.521.

DOI:10.1104/pp.119.2.521
PMID:9952448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC32129/
Abstract

The Arabidopsis mutants eto1 (ethylene overproducer) and eto3 produce elevated levels of ethylene as etiolated seedlings. Ethylene production in these seedlings peaks at 60 to 96 h, and then declines back to almost wild-type levels. Ethylene overproduction in eto1 and eto3 is limited mainly to etiolated seedlings; light-grown seedlings and various adult tissues produce close to wild-type amounts of ethylene. Several compounds that induce ethylene biosynthesis in wild-type, etiolated seedlings through distinct 1-aminocyclopropane-1-carboxylic acid (ACC) synthase (ACS) isoforms were found to act synergistically with eto1 and eto3, as did the ethylene-insensitive mutation etr1 (ethylene resistant), which blocks feedback inhibition of biosynthesis. ACS activity, the rate-limiting step of ethylene biosynthesis, was highly elevated in both eto1 and eto3 mutant seedlings, even though RNA gel-blot analysis demonstrated that the steady-state level of ACS mRNA was not increased, including that of a novel Arabidopsis ACS gene that was identified. Measurements of the conversion of ACC to ethylene by intact seedlings indicated that the mutations did not affect conjugation of ACC or the activity of ACC oxidase, the final step of ethylene biosynthesis. Taken together, these data suggest that the eto1 and eto3 mutations elevate ethylene biosynthesis by affecting the posttranscriptional regulation of ACS.

摘要

拟南芥突变体eto1(乙烯过量产生突变体)和eto3在黄化幼苗阶段产生高水平的乙烯。这些幼苗中的乙烯产量在60至96小时达到峰值,然后回落至几乎野生型水平。eto1和eto3中乙烯的过量产生主要限于黄化幼苗;光照生长的幼苗和各种成年组织产生的乙烯量接近野生型。通过不同的1-氨基环丙烷-1-羧酸(ACC)合酶(ACS)同工型在野生型黄化幼苗中诱导乙烯生物合成的几种化合物,被发现与eto1和eto3协同作用,乙烯不敏感突变体etr1(乙烯抗性)也是如此,它阻断了生物合成的反馈抑制。尽管RNA凝胶印迹分析表明ACS mRNA的稳态水平没有增加,包括一个已鉴定的拟南芥新ACS基因,但在eto1和eto3突变体幼苗中,ACS活性(乙烯生物合成的限速步骤)均显著升高。对完整幼苗中ACC向乙烯转化的测量表明,这些突变不影响ACC的共轭作用或ACC氧化酶(乙烯生物合成的最后一步)的活性。综上所述,这些数据表明eto1和eto3突变通过影响ACS的转录后调控来提高乙烯生物合成。

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