体细胞胚胎发生对于研究早期胚胎发育是细胞和分子机制一个重要的实验模型，尽管来自培养基的外源生长素对体细胞胚胎发生的影响是被人熟知的，但是对于启动体细胞胚的机制还不清楚。本研究表明YUCCAs (YUCs)编码生长素合成的关键酶对于拟南芥SE诱导是必需的。为了发现调控SE启动的其它因素，我们进行了转录水平上的基因表达研究，采用的Affymetrix Arabidopsis Gene Chips的检测服务在博奥生物集团有限公司完成。结果表明参与乙稀合成和反应的基因在SE启动时是下调的。在SE启动阶段，乙烯水平是逐渐下降的，同时ACC处理后或者突变ETHYLENE-OVERPRODUCTION1 (ETO1)会干扰SE诱导，暗示着乙烯在这个过程中发挥了重要作用。在constitutive triple response 1 (ctr1)突变体中也发现SE诱导的抑制，乙烯信号是增加的。不但乙烯合成相关基因下调，而且乙烯反应对于SE诱导是关键的，我们进一步研究了通过抑制YUC表达干扰SE启动表明，或许是局部的生长素合成和生长素的分布的参与。我们的结果为激素调节的SE启动的机制提供了新的信息。本研究于2013年发表在Molecular Plant杂志上（影响因子:6.126）。
Induction of Somatic Embryos in Arabidopsis Requires Local YUCCA Expression Mediated by the Down-Regulation of Ethylene Biosynthesis
Somatic embryogenesis is an important experimental model for studying cellular and molecular mechanisms of early embryo development. Although it has long been known that removal of exogenous auxin from medium results in somatic embryogenesis, the mechanisms underlying the initiation of somatic embryos (SEs) are poorly understood. In this study, we showed that YUCCAs (YUCs) encoding key enzymes in auxin biosynthesis are required for SE induction in Arabidopsis. To identify other factors mediating SE initiation, we performed transcriptional profiling and gene expression analysis. The results showed that genes involved in ethylene biosynthesis and its responses were down-regulated during SE initiation. Ethylene level decreased progressively during SE initiation, whereas treatment with the metabolic precursor of ethylene, 1-aminocyclopropane-1-carboxylic acid (ACC), or mutation of ETHYLENE-OVERPRODUCTION1 (ETO1) disrupted SE induction, suggesting that ethylene plays a role in this process. Suppression of SE induction was also observed in the constitutive triple response 1 (ctr1) mutant, in which ethylene signaling was enhanced. These results indicate that down-regulation of not only ethylene biosynthesis, but also ethylene response is critical for SE induction. We further showed thatethylene disturbed SE initiation through inhibiting YUC expression that might be involved in local auxin biosynthesis and subsequent auxin distribution. Our results provide new information on the mechanisms of hormone-regulated SE initiation.