Dan Hanbin, Yang Guohua, Zheng Zhi-Liang
Department of Biological Sciences, Lehman College, City University of New York, Bronx, NY 10468, USA.
Plant Mol Biol. 2007 Jan;63(2):221-35. doi: 10.1007/s11103-006-9084-0. Epub 2006 Oct 25.
Sulphate is a major macronutrient required for the synthesis of the sulphur (S)-containing amino acid cysteine and thus is critical for cellular metabolism, growth and development and response to various abiotic and biotic stresses. A recent genome-wide expression study suggested that several auxin-inducible genes were up-regulated by S deficiency in Arabidopsis. Here, we examined the relationship between auxin signaling and S deficiency. Investigation of DR5::GUS expression patterns indicates that auxin accumulation and/or response is suppressed by S deficiency. Consistently, S deficiency resulted in the suppression of lateral root development, but the axr1-3 mutant was insensitive to this response. Furthermore, the activation of the promoter for the putative thioglucosidase gene (At2g44460) by S deficiency was suppressed by auxin, cytokinin and abscisic acid (ABA). Interestingly, the activation of At2g44460 by S deficiency is regulated by the availability of carbon and nitrogen nutrients in a tissue-specific manner. These results demonstrate that auxin plays a negative role in signaling to S deficiency. Given that activation of the genes encoding the sulphate transporter SULTR1;2 and 5'-adenylylsulphate reductase APR2 are suppressed by cytokinin only, we hypothesize that while cytokinin may play an important role in general S deficiency response, auxin might be only involved in a subset of S deficiency responses such as the release of thiol groups from the S storage sources.
硫酸盐是合成含硫氨基酸半胱氨酸所需的主要常量营养素,因此对细胞代谢、生长发育以及对各种非生物和生物胁迫的响应至关重要。最近一项全基因组表达研究表明,在拟南芥中,几种生长素诱导基因在硫缺乏时上调。在此,我们研究了生长素信号传导与硫缺乏之间的关系。对DR5::GUS表达模式的研究表明,硫缺乏会抑制生长素的积累和/或响应。一致地,硫缺乏导致侧根发育受到抑制,但axr1-3突变体对此反应不敏感。此外,硫缺乏对假定的硫代葡萄糖苷酶基因(At2g44460)启动子的激活受到生长素、细胞分裂素和脱落酸(ABA)的抑制。有趣的是,硫缺乏对At2g44460的激活受碳和氮营养物质的可用性以组织特异性方式调控。这些结果表明,生长素在硫缺乏信号传导中起负作用。鉴于编码硫酸盐转运蛋白SULTR1;2和5'-腺苷硫酸还原酶APR2的基因的激活仅受细胞分裂素抑制,我们推测,虽然细胞分裂素可能在一般硫缺乏反应中起重要作用,但生长素可能仅参与硫缺乏反应的一个子集,例如从硫储存源释放巯基。