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BYPASS1:移动根衍生信号的合成需要活跃的根生长,并提前阻止叶片发育。

BYPASS1: synthesis of the mobile root-derived signal requires active root growth and arrests early leaf development.

机构信息

Department of Biology, University of Utah, 257 South 1400 East, Salt Lake City, Utah 84112, USA.

出版信息

BMC Plant Biol. 2011 Feb 3;11:28. doi: 10.1186/1471-2229-11-28.

DOI:10.1186/1471-2229-11-28
PMID:21291559
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3045294/
Abstract

BACKGROUND

The Arabidopsis bypass1 (bps1) mutant root produces a biologically active mobile compound that induces shoot growth arrest. However it is unknown whether the root retains the capacity to synthesize the mobile compound, or if only shoots of young seedlings are sensitive. It is also unknown how this compound induces arrest of shoot growth. This study investigated both of these questions using genetic, inhibitor, reporter gene, and morphological approaches.

RESULTS

Production of the bps1 root-synthesized mobile compound was found to require active root growth. Inhibition of postembryonic root growth, by depleting glutathione either genetically or chemically, allowed seedlings to escape shoot arrest. However, the treatments were not completely effective, as the first leaf pair remained radialized, but elongated. This result indicated that the embryonic root transiently synthesized a small amount of the mobile substance. In addition, providing glutathione later in vegetative development caused shoot growth arrest to be reinstated, revealing that these late-arising roots were still capable of producing the mobile substance, and that the older vegetative leaves were still responsive. To gain insight into how leaf development responds to the mobile signal, leaf development was followed morphologically and using the CYCB1,1::GUS marker for G2/M phase cells. We found that arrest of leaf growth is a fully penetrant phenotype, and a dramatic decrease in G2/M phase cells was coincident with arrest. Analyses of stress phenotypes found that late in development, bps1 cotyledons produced necrotic lesions, however neither hydrogen peroxide nor superoxide were abundant as leaves underwent arrest.

CONCLUSIONS

bps1 roots appear to require active growth in order to produce the mobile bps1 signal, but the potential for this compound's synthesis is present both early and late during vegetative development. This prolonged capacity to synthesize and respond to the mobile compound is consistent with a possible role for the mobile compound in linking shoot growth to subterranean conditions. The specific growth-related responses in the shoot indicated that the mobile substance prevents full activation of cell division in leaves, although whether cell division is a direct response remains to be determined.

摘要

背景

拟南芥旁路 1(bps1)突变体的根产生一种具有生物活性的可移动化合物,该化合物诱导芽生长停滞。然而,尚不清楚根是否仍然具有合成该可移动化合物的能力,或者仅幼苗的芽对其敏感。也不知道该化合物如何诱导芽生长停滞。本研究使用遗传、抑制剂、报告基因和形态学方法研究了这两个问题。

结果

发现 bps1 根合成的可移动化合物的产生需要根的活跃生长。通过遗传或化学方法耗尽谷胱甘肽来抑制胚胎后根的生长,使幼苗逃脱芽停滞。然而,这些处理并不完全有效,因为第一对叶仍然是辐射状的,但伸长了。这一结果表明,胚胎根暂时合成了少量的可移动物质。此外,在营养生长后期提供谷胱甘肽会导致芽生长再次停滞,表明这些后期出现的根仍然能够产生可移动物质,并且较老的营养叶仍然有反应。为了深入了解叶片发育如何响应移动信号,我们通过形态学和使用 G2/M 期细胞的 CYCB1,1::GUS 标记物来跟踪叶片发育。我们发现,芽生长停滞是一个完全穿透的表型,与停滞同时出现的是 G2/M 期细胞的急剧减少。对胁迫表型的分析发现,在发育后期,bps1 子叶产生坏死病变,但在叶片停止生长时,过氧化氢和超氧自由基都不丰富。

结论

bps1 根似乎需要活跃生长才能产生移动的 bps1 信号,但在营养生长的早期和晚期都存在合成该可移动化合物的潜力。这种延长的合成和对移动化合物的反应能力与移动化合物在将芽生长与地下条件联系起来的作用一致。芽中的特定生长相关反应表明,该移动物质阻止了叶片中细胞分裂的完全激活,尽管细胞分裂是否是直接反应仍有待确定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/c66b16805e41/1471-2229-11-28-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/694e36e8b818/1471-2229-11-28-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/c7afea7992b4/1471-2229-11-28-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/409a7312f3aa/1471-2229-11-28-3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/dcfc5d4b4bb5/1471-2229-11-28-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/aa91a27bc65b/1471-2229-11-28-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/c66b16805e41/1471-2229-11-28-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/694e36e8b818/1471-2229-11-28-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/c7afea7992b4/1471-2229-11-28-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/409a7312f3aa/1471-2229-11-28-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/f25e23584c34/1471-2229-11-28-4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c79/3045294/c66b16805e41/1471-2229-11-28-7.jpg

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