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A flooding-induced xyloglucan endo-transglycosylase homolog in maize is responsive to ethylene and associated with aerenchyma.

机译:玉米中水淹诱导的木葡聚糖内转糖苷酶同系物对乙烯有反应并与通气组织相关。

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摘要

Development of aerenchyma (soft cortical tissue with large intercellular air spaces) in flooded plants results from cell-wall hydrolysis and eventual cell lysis and is promoted by endogenous ethylene. Despite its adaptive significance, the molecular mechanisms behind aerenchyma development remain unknown. We recently isolated a flooding-induced maize (Zea mays L.) gene (wusl1005[gfu]; abbreviated as 1005) encoding a homolog of xyloglucan endo-transglycosylase (XET), a putative cell-wall-loosening enzyme active during germination, expansion, and fruit softening. XET and related enzymes may also be involved in cell-wall metabolism during flooding-induced aerenchyma development. Under flooding, 1005 mRNA accumulated in root and mesocotyl locations that subsequently exhibited aerenchyma development and reached maximum levels within 12 h of treatment. Aerenchyma development was observed in the same locations by 48 h of treatment. Treatment with the ethylene synthesis inhibitor (aminooxy) acetic acid (AOA), which prevented cortical air space formation under flooding, almost completely inhibited 1005 mRNA accumulation in both organs. AOA treatment had little effect on the accumulation of mRNA encoded by adh1, indicating that it did not cause general suppression of flooding-responsive genes. Additionally, ethylene treatment under aerobic conditions resulted in aerenchyma development as well as induction of 1005 in both organs. These results indicate that 1005 is responsive to ethylene. Treatment with anoxia, which suppresses ethylene accumulation and aerenchyma development, also resulted in 1005 induction. However, in contrast to flooding, AOA treatment under anoxia did not affect 1005 mRNA accumulation, indicating that 1005 is induced via different mechanisms under flooding (hypoxia) and anoxia.
机译:淹没植物中的气孔瘤(具有较大的细胞间空隙的软皮层组织)的发育是由细胞壁水解和最终的细胞裂解引起的,并由内源性乙烯促进。尽管具有适应性意义,但动脉瘤发展背后的分子机制仍然未知。我们最近分离了一个水淹诱导的玉米(Zea mays L.)基因(wusl1005 [gfu];缩写为1005),该基因编码木葡聚糖内转糖基化酶(XET)的同系物,该酶是一种在发芽,扩增过程中活跃的假定的细胞壁松弛酶。和水果软化。 XET和相关酶也可能在水淹诱发的气肿形成过程中参与细胞壁代谢。在淹没下,根和中胚轴位置积聚了1005个mRNA,随后表现出气血发育并在处理后12小时内达到最大水平。通过治疗48小时,在相同位置观察到了气孔形成。用乙烯合成抑制剂(氨氧基)乙酸(AOA)处理可防止淹没时皮层空气空间的形成,几乎完全抑制了两个器官中1005 mRNA的积累。 AOA处理对adh1编码的mRNA的积累几乎没有影响,表明它并未引起泛洪反应基因的普遍抑制。此外,在有氧条件下进行乙烯处理会导致动脉瘤的发展以及在两个器官中诱导产生1005。这些结果表明1005对乙烯有响应。缺氧处理抑制了乙烯的积累和动脉瘤的发展,也导致了1005诱导。然而,与淹没相反,缺氧下的AOA处理不影响1005 mRNA的积累,表明1005是在淹没(缺氧)和缺氧下通过不同的机制诱导的。

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