Control of rice ratooning ability by a nucleoredoxin that inhibits histidine kinase dimerization to attenuate cytokinin signaling in axillary buds

Rice ratooning,the fast outgrowth of dormant buds on stubble,is an important cropping practice in rice production.However,the low ratooning ability(RA)of most rice varieties restricts the application of this cost-efficient system,and the genetic basis of RA remains unknown.In this study,we dissected the genetic architecture of RA by a genome-wide association study in a natural rice population.Rice ratooning ability 3(RRA3),encoding a hitherto not characterized nucleoredoxin involved in reduction of disulfide bonds,was identified as the causal gene of a major locus controlling RA.Overexpression of RRA3 in rice significantly accelerated leaf senescence and reduced RA,whereas knockout of RRA3 significantly delayed leaf senescence and increased RA and ratoon yield.We demonstrated that RRA3 interacts with Oryza sativa histidine kinase 4(OHK4),a cytokinin receptor,and inhibits the dimerization of OHK4 through disulfide bond reduction.This inhibition ultimately led to decreased cytokinin signaling and reduced RA.In addition,variations in the RRA3 promoter were identified to be associated with RA.Introgression of a superior haplotype with weak expression of RRA3 into the elite rice variety Guichao 2 significantly increased RA and ratoon yield by 23.8%.Collectively,this study not only uncovers an undocumented regulatory mechanism of cytokinin signaling through de-dimerization of a histidine kinase receptor-but also provides an eximious gene with promising value for ratoon rice breeding.

Zn^(2+) loading as a critical contributor to the circ_0008553-mediated oxidative stress and inflammation in response to PM_(2.5) exposures

Inflammation is a major adverse outcome induced by inhaled particulate matter with a diameter of≤2.5μm(PM_(2.5)),and a critical trigger ofmost PM_(2.5) exposure-associated diseases.However,the key molecular events regulating the PM_(2.5)-induced airway inflammation are yet to be elucidated.Considering the critical role of circular RNAs(circRNAs)in regulating inflammation,we predicted 11 circRNAs that may be involved in the PM_(2.5)-induced airway inflammation using three previously reportedmiRNAs through the starBasewebsite.A novel circRNA circ_0008553 was identified to be responsible for the PM_(2.5)-activated inflammatory response in human bronchial epithelial cells(16HBE)via inducing oxidative stress.Using a combinatorial model PM_(2.5) library,we found that the synergistic effect of the insoluble core and loaded Zn^(2+)ions at environmentally relevant concentrations was the major contributor to the upregulation of circ_0008553 and subsequent induction of oxidative stress and inflammation in response to PM2.5 exposures.Our findings provided new insight into the intervention of PM_(2.5)-induced adverse outcomes.