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Biology subjects

Teranishi, M.

Publications and source records attributed to Teranishi, M..

2 recordsLinked to original sources

Transfer of cyclobutane pyrimidine dimer photolyase to chloroplasts for Poaceae survival under ultraviolet-B radiation

Cyclobutane pyrimidine dimer (CPD) photolyase (PHR), the primary enzyme for repairing the CPD induced by ultraviolet B (UV-B) radiation, is essential for plants living under sunlight. Rice CPD photolyase (OsPHR), is such a unique triple-targeting protein. The signal sequences required for its translocation to the nucleus or mitochondria are located in the C-terminal region but were yet to be identified for chloroplasts. Here, we identified sequences located in the N-terminal region, including the serine-phosphorylation site at position 7 of OsPHR, and found that OsPHR is transported/localized to chloroplasts via a vesicle transport system under the control of serine phosphorylation. However, the sequence identified in this study is only conserved in some Poaceae species and in many other plants, PHR does not localize to chloroplasts Therefore, we reasoned that Poaceae species need the ability to repair CPD in the chloroplast genome to survive under sunlight and have acquired this new mechanism for chloroplast translocation.

cell biology↗

Increased mitochondrial Ca2+ contributes to health decline with age and Duchene muscular dystrophy in C. elegans.

Sarcopenia is a geriatric syndrome characterized by an age-related decline in skeletal muscle mass and strength. Here, we show that suppression of mitochondrial calcium uniporter (MCU)-mediated Ca2+ influx into mitochondria in the body wall muscles of the nematode Caenorhabditis elegans improved the sarcopenic phenotypes, blunting movement and mitochondrial structural and functional decline with age. We found that normally aged muscle cells exhibited elevated resting mitochondrial Ca2+ levels and increased mitophagy to eliminate damaged mitochondria. Similar to aging muscle, we found that suppressing MCU function in muscular dystrophy improved movement via reducing elevated resting mitochondrial Ca2+ levels. Taken together, our results reveal that elevated resting mitochondrial Ca2+ levels contribute to muscle decline with age and in muscular dystrophy. Further, modulation of MCU activity may act as a potent pharmacological target in various conditions involving muscle loss.

cell biology↗