scholarly journals Evidence for thermosensitivity of the cotton (Gossypium hirsutum L.) immature fiber (im) mutant via hypersensitive stomatal activity

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0259562
Author(s):  
Hee Jin Kim ◽  
Naohiro Kato ◽  
Ruth Ndathe ◽  
Gregory N. Thyssen ◽  
Don C. Jones ◽  
...  

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.

2003 ◽  
Vol 131 (1) ◽  
pp. 264-275 ◽  
Author(s):  
Christelle Dutilleul ◽  
Simon Driscoll ◽  
Gabriel Cornic ◽  
Rosine De Paepe ◽  
Christine H. Foyer ◽  
...  

2020 ◽  
Author(s):  
Gabriele Giachin ◽  
Matthew Jessop ◽  
Romain Bouverot ◽  
Samira Acajjaoui ◽  
Melissa Saidi ◽  
...  

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Tatsuhiro Terada ◽  
Joseph Therriault ◽  
Min Su Peter Kang ◽  
Melissa Savard ◽  
Tharick Ali Pascoal ◽  
...  

Abstract Background Mitochondrial electron transport chain abnormalities have been reported in postmortem pathological specimens of Alzheimer’s disease (AD). However, it remains unclear how amyloid and tau are associated with mitochondrial dysfunction in vivo. The purpose of this study is to assess the local relationships between mitochondrial dysfunction and AD pathophysiology in mild AD using the novel mitochondrial complex I PET imaging agent [18F]BCPP-EF. Methods Thirty-two amyloid and tau positive mild stage AD dementia patients (mean age ± SD: 71.1 ± 8.3 years) underwent a series of PET measurements with [18F]BCPP-EF mitochondrial function, [11C]PBB3 for tau deposition, and [11C] PiB for amyloid deposition. Age-matched normal control subjects were also recruited. Inter and intrasubject comparisons of levels of mitochondrial complex I activity, amyloid and tau deposition were performed. Results The [18F]BCPP-EF uptake was significantly lower in the medial temporal area, highlighting the importance of the mitochondrial involvement in AD pathology. [11C]PBB3 uptake was greater in the temporo-parietal regions in AD. Region of interest analysis in the Braak stage I-II region showed significant negative correlation between [18F]BCPP-EF SUVR and [11C]PBB3 BPND (R = 0.2679, p = 0.04), but not [11C] PiB SUVR. Conclusions Our results indicated that mitochondrial complex I is closely associated with tau load evaluated by [11C]PBB3, which might suffer in the presence of its off-target binding. The absence of association between mitochondrial complex I dysfunction with amyloid load suggests that mitochondrial dysfunction in the trans-entorhinal and entorhinal region is a reflection of neuronal injury occurring in the brain of mild AD.


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