Bolchi A, Petrucco S, Tenca P L, Foroni C, Ottonello S
Institute of Biochemical Sciences, University of Parma, Italy.
Plant Mol Biol. 1999 Feb;39(3):527-37. doi: 10.1023/a:1006148815106.
To gain insight into the regulatory mechanisms and the signals responsible for the adaptation of higher plants to conditions of varying sulfate availability, we have isolated from a sulfate-deprived root library maize cDNAs encoding sulfate permease (ZmST1) and ATP sulfurylase (ZmAS1), the two earliest components of the sulfur assimilation pathway. The levels of ZmST1 and ZmAS1 transcripts concomitantly increased in both roots and shoots of seedlings grown under sulfate-deprived conditions, and rapidly decreased when the external sulfate supply was restored. This coordinate response, which was not observed under conditions of limiting nitrate or phosphate, correlated with the depletion of glutathione, rather than sulfate stores. However, drastically reducing glutathione levels through treatment with buthionine sulfoximine, a specific inhibitor of gamma-glutamyl cysteine synthetase, did not provide an adequate stimulus for the up-regulation of either sulfate permease or ATP sulfurylase messengers. Indeed, L-cysteine, but not D-cysteine, effectively down-regulated both transcripts when supplied to sulfur-deficient seedlings under conditions of blocked glutathione synthesis. Altogether, these data provide evidence for the coordinate regulation of sulfur assimilation mRNAs in higher plants and for the glutathione-independent involvement of cysteine as a stereospecific pretranslational modulator of the expression of sulfur status-responsive genes.
为深入了解高等植物适应不同硫酸盐可利用性条件的调控机制和相关信号,我们从一个硫酸盐缺乏的根文库中分离出了编码硫酸盐转运蛋白(ZmST1)和ATP硫酸化酶(ZmAS1)的玉米cDNA,这两者是硫同化途径中最早的两个组分。在硫酸盐缺乏条件下生长的幼苗的根和芽中,ZmST1和ZmAS1转录本水平同时升高,而当恢复外部硫酸盐供应时则迅速下降。这种协同反应在硝酸盐或磷酸盐限制条件下未观察到,它与谷胱甘肽的消耗相关,而非硫酸盐储备。然而,用丁硫氨酸亚砜胺(一种γ-谷氨酰半胱氨酸合成酶的特异性抑制剂)处理大幅降低谷胱甘肽水平,并未为硫酸盐转运蛋白或ATP硫酸化酶信使的上调提供足够的刺激。实际上,在谷胱甘肽合成受阻的条件下,向缺硫幼苗供应L-半胱氨酸而非D-半胱氨酸时,能有效下调这两种转录本。总之,这些数据为高等植物中硫同化mRNA的协同调控以及半胱氨酸作为硫状态响应基因表达的立体特异性翻译前调节剂的谷胱甘肽非依赖性参与提供了证据。