LHT1/MAC7 contributes to proper alternative splicing under long-term heat stress and mediates the variation in the tolerance of Arabidopsis
Natural genetic variation has facilitated the identification of genes underlying complex traits such as stress tolerances. We here evaluated the long-term (L-) heat tolerance (37 oC for 5 days) of 174 Arabidopsis thaliana accessions and found a nearly ten-fold variation in the tolerance among them. To elucidate the variation in L-heat tolerance and the underling mechanisms of A. thaliana accessions, we performed a chromosomal mapping using the F2 progeny of an Ms-0 (hyper-sensitive accession) and Col-0 (tolerant accession) cross and found a single locus responsible for the variation in L-heat tolerance between Ms-0 and Col-0, which named Long-term Heat Tolerance1 (LHT1). LHT1 is identical to MAC7, encoding a putative RNA helicase, involved in mRNA splicing as a component of MOS4 complex. We found one amino acid deletion in LHT1, which causes a loss of LHT1 function of Ms-0. The mos4-2, cdc5-1, mac3a mac3b, prl1 prl2, which are core components of MOS4 complex showed hyper-sensitivity to L-heat stress compared to WT, suggesting that the MOS4 complex plays an important role in L-heat stress responses. The L-heat stress induced mRNA processing-related genes and affected in the alternative splicing. Loss of LHT1 function genome-widely caused detrimental splicing events, which are thought to produce non-functional mRNAs including retained introns under L-heat stress. These findings suggest that maintaining proper alternative splicing under L-heat stress is important in the tolerance of A. thaliana.