Tamura Shun, Yoshimura Etsuro
Department of Applied Biological Chemistry, School of Agriculture and Life Sciences, The University of Tokyo, Tokyo, 113-8657, Japan.
Biol Trace Elem Res. 2008 Sep;124(3):262-8. doi: 10.1007/s12011-008-8145-4. Epub 2008 May 8.
A Saccharomyces cerevisiae mutant (zrt1Delta) lacking the ZRT1 gene, which encodes a high-affinity Zn(2+) transporter, scarcely thrived in a low-pH, low-phosphate medium because of Zn(2+) deficiency. Supplementation of the medium with Al(3+) restored growth to a level comparable to that of a wild-type strain. A metal determination study clearly demonstrated that Al(3+) induced the incorporation of Zn(2+) into zrt1Delta cells, probably through the low-affinity Zn(2+) transporter Zrt2p, given that the zrt1Deltazrt2Delta double mutant did not show Al-induced growth enhancement. Al(3+) may have altered the speciation of Zn(2+) in the medium, resulting in enhanced levels of free Zn(2+). Alternatively, it might be that Zrt2p was degraded by endocytosis in the absence of Al(3+) and Al(3+) interfered with this process, resulting in enhanced Zn(2+) accumulation.
酿酒酵母的一个突变体(zrt1Delta)缺乏编码高亲和力锌离子转运蛋白的ZRT1基因,由于锌离子缺乏,它在低pH、低磷酸盐培养基中几乎无法生长。向培养基中添加铝离子可使生长恢复到与野生型菌株相当的水平。一项金属测定研究清楚地表明,铝离子可能通过低亲和力锌离子转运蛋白Zrt2p诱导锌离子进入zrt1Delta细胞,因为zrt1Deltazrt2Delta双突变体没有表现出铝诱导的生长增强。铝离子可能改变了培养基中锌离子的形态,导致游离锌离子水平升高。或者,可能是在没有铝离子的情况下,Zrt2p通过内吞作用被降解,而铝离子干扰了这一过程,导致锌离子积累增加。