MOS4-associated complex contributes to proper splicing and suppression of ER stress under long-term heat stress in Arabidopsis.

Abstract

Plants are often exposed not only to short-term (S-) but also to long-term (L-)heat stress over several consecutive days. A few Arabidopsis mutants defective in L-heat tolerance have been identified, but the molecular mechanisms are less understood for this tolerance than for S-heat stress tolerance. To elucidate the mechanisms of the former, we used a forward genetic screen for <i>sensitive to long-term heat</i> (<i>sloh</i>) mutants and isolated <i>sloh3</i> and <i>sloh63</i>. The mutants were hypersensitive to L- but not to S-heat stress, and <i>sloh63</i> was also hypersensitive to salt stress. We identified the causal genes, <i>SLOH3</i> and <i>SLOH63</i>, both of which encoded splicing-related components of the MOS4-associated complex (MAC). This complex is widely conserved in eukaryotes and has been suggested to interact with spliceosomes. Both genes were induced by L-heat stress in a time-dependent manner, and some abnormal splicing events were observed in both mutants under L-heat stress. In addition, endoplasmic reticulum (ER) stress and subsequent unfolded protein response occurred in both mutants under L-heat stress and were especially prominent in <i>sloh63</i>, suggesting that enhanced ER stress is due to the salt hypersensitivity of <i>sloh63</i>. Splicing inhibitor pladienolide B led to concentration-dependent disturbance of splicing, decreased L-heat tolerance, and enhanced ER stress. These findings suggest that maintenance of precise mRNA splicing under L-heat stress by the MAC is important for L-heat tolerance and suppressing ER stress in Arabidopsis.