Body of Abstract: Thickness of cotton fiber is referred to as fiber maturity. Fiber maturity is a key determinant of fiber quality, lint yield and textile performance. We used the cotton immature fiber (im) mutant to understand how 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 first characterized growth and gas exchange in im and TM-1 under no stress. Then we compared gas exchange and transcriptomic profiles of the two NILs under high temperature. Under no stress, phenotypic differences were detected between the NILs in non-fiber tissues also although less pronounced than in fibers. At near optimum temperature (28+3oC), im maintained the same photosynthetic performance as TM-1 by means of greater stomatal conductance and higher chlorophyll content. In contrast, under high temperature stress ( >34oC), 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 theim mutant previously reported to have low activity of mitochondrial complex I displays increased thermosensitivity by impacting stomatal conductance. Reduced photosynthesis in ambient temperatures above 34oC may play a role in causing the im phenotype. Results also support the 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.