激活的HD-START蛋白增强拟南芥抗旱能力:根系与气孔调控

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在研究植物对干旱耐受性的基础机制以及寻找改良这一关键性农业特性基因的过程中,研究人员通过对拟南芥(Arabidopsis thaliana)进行转基因筛选,发现了一种名为"增强干旱耐受1"的突变体。这种突变体展现出显著的干旱抵抗能力,其主要表现在以下几个方面: 首先,与野生型相比,增强干旱耐受1的植株具有更发达的根系统。突变株的根系更深且侧根数量增多,这有利于植物在干旱条件下更有效地获取水分,增强水分利用效率。根部结构的改进是植物对干旱环境适应的重要策略。 其次,突变体的叶片气孔密度较低。气孔是植物蒸腾作用的通道,降低气孔密度可以减少水分蒸发,有助于植物在缺水状态下保持水分平衡,从而提高干旱耐受性。 此外,增强干旱耐受1植株表现出更高的脱落酸(ABA)和脯氨酸(Pro)含量。ABA是一种植物激素,在干旱等逆境胁迫下起着调节植物生理反应的关键作用,脯氨酸则作为渗透调节物质,帮助植物细胞抵抗脱水。这些变化表明,该突变体可能通过调控这些激素的水平来增强对干旱的响应。 在分子遗传学分析中,科学家们发现突变是由一个被T-DNA标签编码的潜在转录因子——homeodomain-START基因的激活表达所导致的。homeodomain-START转录因子被认为在植物生长发育和应答逆境信号过程中发挥重要作用。激活表达意味着这个因子在正常情况下可能未达到完全活性,而在突变体中由于某种机制被增强,从而促进了干旱耐受性。 为了验证这一发现,研究者将该转录因子的cDNA过量表达在烟草转基因植株中,结果发现这些转基因植物同样显示出干旱耐受性,并伴有改进的根系结构和降低的气孔密度,进一步证实了该转录因子在调控植物干旱耐受性中的核心作用。 通过激活表达一个homeodomain-START转录因子,研究人员揭示了其在干旱耐受性中的新功能,并为改善植物对干旱环境的适应提供了重要的遗传调控靶点。这一研究对于作物育种具有重要意义,未来有可能通过遗传工程技术将这种耐旱机制应用到农作物中,提高农业生产在干旱条件下的稳定性。

Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.请用nature杂志的风格润色成学术论文的形式。

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