Abstract:
The mechanisms of plant drought resistance are unclear but may involve membrane trafficking and metabolic reprogramming, including proline accumulation. Forward genetic screening using a proline dehydrogenase 1 (ProDH1) promoter:reporter identified a drought hypersensitive mutant with a single-amino acid substitution (P335L) in the nonphototrophic hypocotyl 3 (NPH3) domain of NPH3/root phototropism 2-like 5 (NRL5)/naked pins in Yucca 8 (NPY8). Further experiments found that NRL5 and other NPH3 domain proteins are guanosine triphosphatases (GTPases). NRL5, but not NRL5P335L, interacted with the RABE1c and RABH1b GTPases and the soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) Vesicle-Associated Membrane Protein (VAMP)721/722. These proteins controlled NRL5 localization and connection to trafficking while also being genetically downstream of, and potentially regulated by, NRL5. These data demonstrate that NRL5-mediated restraint of proline catabolism is required for drought resistance and also reveal unexpected functions of the NPH3 domain such that the role of NPH3 domain proteins in signaling, trafficking, and cellular polarity can be critically reevaluated.
摘要:
植物抗旱机制尚不清楚,但可能涉及膜运输和代谢重编程,包括脯氨酸的积累。使用脯氨酸脱氢酶1(ProDH1)启动子进行正向遗传筛选:报告分子在NPH3/根向光性2样5(NRL5)的非光养性下胚轴3(NPH3)结构域中鉴定出一个单氨基酸取代(P335L)的干旱超敏突变体。丝兰8(NPY8)的裸针。进一步的实验发现NRL5和其他NPH3结构域蛋白是鸟苷三磷酸酶(GTP酶)。NRL5,但不是NRL5P335L,与RABE1c和RABH1bGTP酶以及可溶性N-乙基马来酰亚胺敏感因子附着蛋白受体(SNAREs)囊泡相关膜蛋白(VAMP)721/722相互作用。这些蛋白质控制NRL5的定位和与贩运的联系,同时也在基因下游,并可能受到监管,NRL5。这些数据表明,NRL5介导的脯氨酸分解代谢抑制是抗旱所必需的,并且还揭示了NPH3结构域的意外功能,例如NPH3结构域蛋白在信号传导中的作用。贩运,和细胞极性可以批判性地重新评估。