楔叶铁线蕨孢子组织培养技术研究

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"以孢子为外植体的楔叶铁线蕨组织培养 (2008年) - 田晓艳、刘延吉叶、王妹2 - 食品与生物技术学报" 这篇论文主要探讨了使用楔叶铁线蕨(A. raddianum)的孢子作为外植体进行组织培养的技术。组织培养是一种通过无菌条件下对植物细胞、组织或器官进行培养,以快速繁殖和遗传改良植物的技术。在本文中,研究者关注的是如何优化培养条件以促进孢子的萌发和孢子体的诱导。 首先,孢子初代培养阶段的研究表明,低无机盐含量的基本培养基对于孢子萌发最为适宜。这可能是因为较低的无机盐浓度可以减少对孢子的刺激,提供一个较为温和的环境,有利于孢子的正常发育。 接着,孢子体萌发阶段的最佳培养基配置被确定为1/2MS培养基,结合3.0 mg/L的赤霉素(GA)、0.3 g/dL的活性炭、30 g/L的蔗糖和0.65 g/dL的琼脂,pH值保持在5.8至6.0之间。赤霉素是一种植物生长调节剂,能刺激细胞伸长,促进萌发。活性炭则可能用于吸附培养基中的有害物质,改善培养环境。蔗糖作为碳源,提供能量,而琼脂则作为凝固剂使培养基保持固体状态。 在原叶体增殖阶段,最佳的培养基组合为1/3MS培养基,配合2.0 mg/L的萘乙酸(NAA)、30 g/L蔗糖和0.65 g/dL琼脂,同样保持pH值在5.8至6.0。萘乙酸是另一种生长调节剂,常用于促进植物根系的形成和生长。 最后,孢子体的诱导采用了不完全组织培养,即使用珍珠岩:蛙石:苹果炭土以1:1:1比例混合的基质。这种方式可能旨在模拟更接近自然环境的生长条件,有利于孢子体的进一步发育和适应性。 关键词包括铁线蕨、孢子、快繁、组织培养和孢子体诱导,表明这项研究的目标是建立一个快速繁殖铁线蕨的组织培养系统,并特别关注孢子阶段的处理和诱导。 这篇论文详细阐述了利用孢子进行楔叶铁线蕨组织培养的各个步骤和优化条件,为该物种的快速繁殖和遗传研究提供了科学依据。通过这些优化的培养条件,研究者能够有效地控制和促进铁线蕨的生长,这对于植物繁殖、种群恢复以及种质资源保存具有重要意义。

帮我把下面这段英文从用词、语法、结构上修改一下。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.

2023-02-10 上传

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.

2023-02-10 上传