Genome sequence of aod2 mutant derived from Arabidopsis thaliana Bu-5

Acquired osmotolerance induced after salt stress is widespread across Arabidopsis thaliana (Arabidopsis) accessions including Bu-5. However, it remains unclear how the osmotolerance is established. We isolated an acquired osmotolerance-defective mutant 2 (aod2) from ion beam-mutagenized M2 population of Bu-5. The aod2 was impaired not only in acquired osmotolerance, but also in osmo-shock, salt-shock and long-term (L-) heat tolerances compared to WT and displayed abnormal morphology, including wrinkled small leaves and zigzag stems. We found that the 439 kbp region of chromosome 4 was translocated into the causal locus for the osmosensitive phenotype of aod2 on chromosome 3. The causal gene of aod2 was identical to ECERIFERUM 10 (CER10) encoding an enoyl-CoA reductase involved in very-long-chain fatty acids (VLCFA) elongation reactions required for cuticular wax, storage lipid, and sphingolipid metabolism.

盐胁迫诱导的获得性渗透耐受性（acquired osmotolerance）在包括Bu-5在内的拟南芥（Arabidopsis thaliana，简称Arabidopsis）生态型中广泛存在。然而，目前仍未明确该获得性渗透耐受性的建立机制。我们从Bu-5的离子束诱变M2群体中分离得到一株获得性渗透耐受缺陷突变体2（aod2）。与野生型（WT）相比，aod2不仅在获得性渗透耐受性方面存在缺陷，同时在渗透冲击、盐冲击及长期（L-）热耐受性上均受损，且表现出皱缩小叶、曲折茎秆等异常形态。我们发现，4号染色体上一段439 kbp的区域易位至3号染色体上与aod2渗透敏感表型相关的因果位点。aod2的因果基因与ECERIFERUM 10（CER10）完全一致，该基因编码一种烯酰辅酶A还原酶（enoyl-CoA reductase），参与调控表皮蜡质、贮藏脂质及鞘脂代谢所需的超长链脂肪酸（VLCFA）延伸反应。