USDA-ARS, Southern Regional Research Center, Cotton Fiber Bioscience Research Unit, New Orleans, LA, United States of America.
Department of Biological Sciences, Louisiana State University, Baton Rouge, LA, United States of America.
PLoS One. 2021 Dec 13;16(12):e0259562. doi: 10.1371/journal.pone.0259562. eCollection 2021.
Thickness of cotton fiber, referred to as fiber maturity, is a key determinant of fiber quality, lint yield, and textile performance. The cotton immature fiber (im) mutant has been used to study fiber maturity since its fiber is thinner than the wild type near isogeneic line (NIL), Texas Marker-1 (TM-1). The im phenotype is caused by a single recessive mutation of a pentatricopeptide repeat (PPR) gene that reduces the activity of mitochondrial complex I and up-regulates stress responsive genes. However, the mechanisms altering the stress responses in im mutant are not well understood. Thus, we characterized growth and gas exchange in im and TM-1 under no stress and also investigated their stress responses by comparing gas exchange and transcriptomic profiles under high temperature. Phenotypic differences were detected between the NILs in non-fiber tissues although less pronounced than the variation in fibers. At near optimum temperature (28±3°C), im maintained the same photosynthetic performance as TM-1 by means of greater stomatal conductance. In contrast, under high temperature stress (>34°C), im leaves reduced photosynthesis by decreasing the stomatal conductance disproportionately more than TM-1. Transcriptomic analyses showed that the genes involved in heat stress responses were differentially expressed between the NIL leaves. These results indicate that the im mutant previously reported to have low activity of mitochondrial complex I displays increased thermosensitivity by impacting stomatal conductance. They also support a notion that mitochondrial complex I activity is required for maintenance of optimal photosynthetic performance and acclimation of plants to high temperature stress. These findings may be useful in the future efforts to understand how physiological mechanisms play a role in determining cotton fiber maturity and may influence stress responses in other crops.
棉纤维的厚度，称为纤维成熟度，是纤维质量、皮棉产量和纺织性能的关键决定因素。棉花未成熟纤维（im）突变体由于其纤维比近等基因系（NIL）德克萨斯标记-1（TM-1）的野生型更细，因此一直被用于研究纤维成熟度。im 表型是由一个五肽重复（PPR）基因的单个隐性突变引起的，该突变降低了线粒体复合物 I 的活性并上调了应激响应基因。然而，改变 im 突变体应激响应的机制尚不清楚。因此，我们在无胁迫条件下对 im 和 TM-1 的生长和气体交换进行了表征，并通过比较高温下的气体交换和转录组谱来研究它们的应激响应。尽管在纤维中的变化不那么明显，但在非纤维组织中，NIL 之间存在表型差异。在接近最佳温度（28±3°C）下，im 通过更大的气孔导度维持与 TM-1 相同的光合作用性能。相比之下，在高温胁迫下（>34°C），im 叶片通过不成比例地减少气孔导度来减少光合作用，而 TM-1 则减少得较少。转录组分析表明，与 NIL 叶片中热应激响应相关的基因表达存在差异。这些结果表明，先前报道的线粒体复合物 I 活性较低的 im 突变体通过影响气孔导度表现出更高的热敏性。它们还支持这样一种观点，即线粒体复合物 I 活性对于维持最佳光合作用性能和植物对高温胁迫的适应是必需的。这些发现可能有助于未来理解生理机制在决定棉花纤维成熟度方面的作用，并可能影响其他作物的应激响应。
