Yeast genes involved in response to lactic acid and acetic acid:: acidic conditions caused by the organic acids in Saccharomyces cerevisiae cultures induce expression of intracellular metal metabolism genes regulated by Aft1p
Yeast genes involved in response to lactic acid and acetic acid:: acidic conditions caused by the organic acids in Saccharomyces cerevisiae cultures induce expression of intracellular metal metabolism genes regulated by Aft1p
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DOI：
10.1111/j.1567-1364.2006.00089.x
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发表时间：
2006-09-01
影响因子：
3.2
通讯作者：
Iefuji, Haruyuki
中科院分区：
文献类型：
--
作者：
Kawahata, Miho;Masaki, Kazuo;Iefuji, Haruyuki
使用两种类型的全基因组分析来研究与乳酸和乙酸反应有关的酵母基因，我们发现酸性条件会影响金属代谢。第一种类型是使用 DNA 微阵列进行表达分析，以研究“酸休克反应”作为适应酸性条件的第一步，以及通过维持酸性条件下的完整性来研究“酸适应”。另一种是使用酿酒酵母的非必需基因缺失集合进行功能筛选。表达分析表明，参与应激反应的基因，如YGP1、TPS1和HSP150，在酸休克反应下被诱导表达。 FIT2、ARN1 和 ARN2 等参与 Aft1p 调节的金属代谢的基因在酸适应下被诱导。 AFT1 在酸休克反应和乳酸酸适应下被诱导。此外，在含有乳酸、乙酸或盐酸的培养基中生长的细胞中，绿色荧光蛋白融合的 Aft1p 定位于细胞核。两项分析都表明酸性条件影响细胞壁结构。 SED1、DSE2、CTS1、EGT2、SCW11、SUN4 和 YNL300W 编码的细胞壁成分以及 YID21、EAF3、EAF5、EAF6 和 YAF9 编码的组蛋白乙酰转移酶复合体蛋白的消耗增加了对乳酸的抵抗力。尽管 SED1 的表达是通过暴露于乳酸而诱导的，但细胞壁甘露糖蛋白 Sed1p 的消耗提供了对乳酸的抵抗力。液泡膜 H+-ATP 酶和高渗透性甘油丝裂原激活蛋白激酶蛋白的消耗导致酸敏感性。此外，我们的定量PCR表明，PDR12的表达在乳酸酸休克反应下增加，而在盐酸酸适应下减少。
Using two types of genome-wide analysis to investigate yeast genes involved in response to lactic acid and acetic acid, we found that the acidic condition affects metal metabolism. The first type is an expression analysis using DNA microarrays to investigate 'acid shock response' as the first step to adapt to an acidic condition, and 'acid adaptation' by maintaining integrity in the acidic condition. The other is a functional screening using the nonessential genes deletion collection of Saccharomyces cerevisiae. The expression analysis showed that genes involved in stress response, such as YGP1, TPS1 and HSP150, were induced under the acid shock response. Genes such as FIT2, ARN1 and ARN2, involved in metal metabolism regulated by Aft1p, were induced under the acid adaptation. AFT1 was induced under acid shock response and under acid adaptation with lactic acid. Moreover, green fluorescent protein-fused Aft1p was localized to the nucleus in cells grown in media containing lactic acid, acetic acid, or hydrochloric acid. Both analyses suggested that the acidic condition affects cell wall architecture. The depletion of cell-wall components encoded by SED1, DSE2, CTS1, EGT2, SCW11, SUN4 and YNL300W and histone acetyltransferase complex proteins encoded by YID21, EAF3, EAF5, EAF6 and YAF9 increased resistance to lactic acid. Depletion of the cell-wall mannoprotein Sed1p provided resistance to lactic acid, although the expression of SED1 was induced by exposure to lactic acid. Depletion of vacuolar membrane H+-ATPase and high-osmolarity glycerol mitogen-activated protein kinase proteins caused acid sensitivity. Moreover, our quantitative PCR showed that expression of PDR12 increased under acid shock response with lactic acid and decreased under acid adaptation with hydrochloric acid.