585 / 2019-04-30 14:39:42

Dysfunction of sterol 4α-methyl oxidase1 (SMO1) in Arabidopsis leads to embryo lethal and twin embryos

sterol, embyo, sterol 4α-methyl oxidase, development

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Phytosterols play important roles in plant growth and development (Schaller H. 2003). Plant sterol biosynthesis differs with that of fungi and mammals in the removal of the two methyl groups at C-4 position. In mammals and fungi, the two C4-methyls are removed consecutively by the same set of enzyme complex including a sterol 4α-methyl oxidase (SMO), a 4α-carboxysterol-C-3-dehydrogenase/C4-decarboxylase (CSD), a sterone ketoreductase (SKR) and a scaffold protein ERG28, whereas in plants the two C4-demethylations are interrupted by four other enzymatic steps, and there are two distinct SMOs (SMO1 and SMO2) with respective substrate specificity (Darnet and Rahier 2004). In Arabidopsis, there are three SMO1 and two SMO2 genes, respectively. In our previous report we found that smo2-1 som2-2 was embryo lethal, and its embryo abortion phenotype could be partially rescued by auxin application or endogenous auxin overproduction (Zhang et al., 2016). However, SMO1s function in embryo development remains unclear. In our present study, we found that smo1-1 smo1-2 double mutant was also embryo lethal, but its phenotype was more severe than those of smo2-1 som2-2. Moreover, smo1-1 smo1-2 embryos displayed two novel phenotypes: (1) There were longitudinal divisions in the suspensor cells, which resulted in thick suspensor with multi cell layers in girth; (2) Some smo1-1 smo1-2 seeds contained twin embryos. We are now trying to decipher the underline mechanism of these embryo phenotypes.