树生物 (Rhizobium meliloti) 的共生突变,使植物从细菌分化中脱离
Cell
|April 1, 1985
概括
自发的Rhizobium meliloti突变缺乏外聚糖在没有感染线程的柳上形成结节. 这些缺乏固化的 (固定的) 结节表明,感染线程对于结节的形成并不必不可少.
科学领域:
- 微生物学 微生物学
- 植物 - 细菌共生体
- 分子遗传学 分子遗传学
背景情况:
- Rhizobium meliloti SU47与树形成共生关系,这对固有至关重要.
- 外聚糖 (EPS) 在共生的早期阶段发挥作用,包括根发和感染线程形成.
- 在结节的发展和功能中EPS和感染线程的确切作用尚未完全理解.
研究的目的:
- 为了研究缺乏外聚糖的自发Rhizobium meliloti突变体的共生表型.
- 为了确定感染线程的必要性,以形成结和发展在 - 生菌共生.
- 探索细菌信号在启动结节发育的作用,独立于感染.
主要方法:
- 隔离和特征自发的Rhizobium meliloti SU47突变,表现出改变的表面特性 (菌体耐药性,抗体不敏感性).
- 用突变菌株接种时草根结节的形成和发展的表型分析.
- 结节结构的显微镜检查,包括感染线和细菌定位.
- 评估由突变菌株形成的结节中的固能力.
主要成果:
- 突变者缺乏野生类型的外聚糖,导致表面特征发生变化.
- 突变菌株在没有根毛或可见的感染线索的情况下,在上启动了结节的形成.
- 突变者形成的结节在表面细胞间空间中含有细菌,缺乏bacteroids,并且缺乏固定 (Fix-).
- 有证据表明,细菌信号可以诱导结节的形成,独立于感染线程和细菌分化.
结论:
- 感染线程对于启动细胞增殖和结形成在 - 生菌共生中并不重要.
- 一个细菌信号可以在远处触发结节的发展,与细菌分化的正常过程脱离.
- 在Rhizobium meliloti中,外聚糖缺乏改变了共生相互作用,突出了它在初始感染之外的复杂作用.
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