The ultraviolet B (UVB) sensitivity of rice cultivated in Asia and Africa varies greatly, with African rice cultivars (Oryza glaberrima Steud. and O. barthii A. Chev.) being more sensitive to UVB because of their low cyclobutane pyrimidine dimer (CPD) photolyase activity, which is a CPD repair enzyme, relative to Asian rice cultivars (O. sativa L.). Hence, the production of UVB-resistant African rice with augmented CPD photolyase activity is of great importance, although difficulty in transforming the African rice cultivars to this end has been reported. Here, we successfully produced overexpressing transgenic African rice with higher CPD photolyase activity by modifying media conditions for callus induction and regeneration using the parental line (PL), UVB-sensitive African rice TOG12380 (O. glaberrima). The overexpressing transgenic African rice carried a single copy of the CPD photolyase enzyme, with a 4.4-fold higher level of CPD photolyase transcripts and 2.6-fold higher activity than its PL counterpart. When the plants were grown for 21 days in a growth chamber under visible radiation or with supplementary various UVB radiation, the overexpressing transgenic plants have a significantly increased UVB resistance index compared to PL plants. These results strongly suggest that CPD photolyase remains an essential factor for tolerating UVB radiation stress in African rice. As a result, African rice cultivars with overexpressed CPD photolyase may survive better in tropical areas more prone to UVB radiation stress, including Africa. Collectively, our results provide strong evidence that CPD photolyase is a useful biotechnological tool for reducing UVB-induced growth inhibition in African rice crops of O. glaberrima.

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 Ca ²⁺ 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 Ca ²⁺ 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 Ca ²⁺ levels. Taken together, our results reveal that elevated resting mitochondrial Ca ²⁺ levels contribute to muscle decline with age and muscular dystrophy. Further, modulation of MCU activity may act as a potential pharmacological target in various conditions involving muscle loss.

The suppressor of gamma response 1 (SOG1), a NAM, ATAF1, 2, and CUC2 (NAC)‐type transcription factor found in seed plants, is a master regulator of DNA damage responses (DDRs). Upon DNA damage, SOG1 regulates the expression of downstream DDR genes. To know the origin of the DDR network in land plants, we searched for a homolog(s) of SOG1 in a moss Physcomitrium (Physcomitrella) patens and identified PpSOG1a and PpSOG1b. To assess if either or both of them function(s) in DDR, we knocked out the PpSOG1s using CRISPR/Cas9‐mediated gene editing and analyzed the responses to DNA‐damaging treatments. The double‐knockout (KO) sog1a sog1b plants showed resistance to γ‐rays, bleomycin, and ultraviolet B (UVB) treatments similarly seen in Arabidopsis sog1 plants. Next, we irradiated wild‐type (WT) and KO plants with γ‐rays and analyzed the whole transcriptome to examine the effect on the expression of DDR genes. The results revealed that many P. patens genes involved in the checkpoint, DNA repair, replication, and cell cycle‐related genes were upregulated after γ‐irradiation, which was not seen in sog1a sog1b plant. These results suggest that PpSOG1a and PpSOG1b work redundantly on DDR response in P. patens; in addition, plant‐specific DDR systems had been established before the emergence of vascular plants.

Various environmental factors control the plant flowering time. However, the specific effects of ultraviolet (UV)‐B radiation on flowering remain unclear. UV‐B irradiation delays flowering in Arabidopsis during short‐day (SD) photoperiods. In contrast, UV‐B irradiation causes a variety of flowering phenotypes during long‐day (LD) photoperiods, including unchanged, delayed, and accelerated flowering. We hypothesized that variations in UV‐B intensity are responsible for the phenotypic changes under LD photoperiods. Therefore, in this study, Arabidopsis plants were exposed to two distinct UV‐B intensities: a low UV‐B intensity that activates UVR8‐dependent pathways and high UV‐B intensity that activates both UVR8‐dependent and ‐independent pathways. Under LD photoperiods, neither the wild‐type (WT) nor the uvr8 mutant showed any change in flowering time at either UV‐B irradiation intensity. Under the SD photoperiod, UV‐B irradiation delayed WT flowering. The expression of flowering locus T ( FT ) increased after UV‐B irradiation under the LD photoperiod in a UVR8‐dependent manner. However, despite the increased expression of FT , expression levels of floral meristem identity genes in shoot apical meristem (SAM) were not increased by UV‐B irradiation. As UV‐B irradiation is known to suppress flowering in SAM in a UVR8‐dependent manner, increase in FT expression induced by UV‐B irradiation possibly antagonized the suppressive effect of UV‐B irradiation. Overall, these results suggest that flowering phenotypes do not change with UV‐B intensity but with the balance between the inhibitory and promotive effects of UVR8 activated by UV‐B irradiation.

Photoreactivation enzyme that repairs cyclobutane pyrimidine dimer (CPD) induced by ultraviolet-B radiation, commonly called CPD photolyase (PHR) is essential for plants living under sunlight. Rice (Oryza sativa) PHR (OsPHR) is 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 have 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 is not localized to the chloroplasts. Therefore, we reasoned that Poaceae species need the ability to repair CPD in the chloroplast genome to survive under sunlight and have uniquely acquired this mechanism for PHR chloroplast translocation.

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.