Domestication has resulted in reduced salt tolerance in tomato. To identify the genetic components causing this deficiency, we performed a genome-wide association study (GWAS) for root Na + /K + ratio in a population consisting of 369 tomato accessions with large natural variations. The most significant variations associated with root Na + /K + ratio were identified within the gene SlHAK20 encoding a member of the clade IV HAK/KUP/KT transporters. We further found that SlHAK20 transports Na + and K + and regulates Na + and K + homeostasis under salt stress conditions. A variation in the coding sequence of SlHAK20 was found to be the causative variant associated with Na + /K + ratio and confer salt tolerance in tomato. Knockout mutations in tomato SlHAK20 and the rice homologous genes resulted in hypersensitivity to salt stress. Together, our study uncovered a previously unknown molecular mechanism of salt tolerance responsible for the deficiency in salt tolerance in cultivated tomato varieties. Our findings provide critical information for molecular breeding to improve salt tolerance in tomato and other crops.

The widespread agricultural problem of pre-harvest sprouting (PHS) could potentially be overcome by improving seed dormancy. Here, we report that miR156, an important grain yield regulator, also controls seed dormancy in rice. We found that mutations in one MIR156 subfamily enhance seed dormancy and suppress PHS with negligible effects on shoot architecture and grain size, whereas mutations in another MIR156 subfamily modify shoot architecture and increase grain size but have minimal effects on seed dormancy. Mechanistically, mir156 mutations enhance seed dormancy by suppressing the gibberellin (GA) pathway through de-represssion of the miR156 target gene Ideal Plant Architecture 1 ( IPA1 ), which directly regulates multiple genes in the GA pathway. These results provide an effective method to suppress PHS without compromising productivity, and will facilitate breeding elite crop varieties with ideal plant architectures.

Terrestrial plants must cope with drought stress to survive. Under drought stress, plants accumulate the phytohormone abscisic acid (ABA) by increasing its biosynthesis and decreasing its catabolism. However, the regulatory pathways controlling ABA catabolism in response to drought remain largely unclear. Here, we report that the flowering repressor SHORT VEGETATIVE PHASE (SVP) is induced by drought stress and associates with the promoter regions of the ABA catabolism pathway genes CYP707A1, CYP707A3 and AtBG1, causing decreased expression of CYP707A1 and CYP707A3 but enhanced expression of AtBG1 in Arabidopsis leaves. Loss-of-function mutations in CYP707A1 and CYP707A3 or overexpression of AtBG1 could rescue the drought-hypersensitive phenotype of svp mutant plants by increasing cellular ABA levels. Collectively, our results suggest that SVP is a central regulator of ABA catabolism and that a regulatory pathway involving SVP, CYP707A1/3, and AtBG1 plays a critical role in plant response to water deficit and plant drought resistance.