An atypical PMR2 locus is responsible for hypersensitivity to sodium and lithium cations in the laboratory strain Saccharomyces cerevisiae CEN.PK113-7D
An atypical PMR2 locus is responsible for hypersensitivity to sodium and lithium cations in the laboratory strain Saccharomyces cerevisiae CEN.PK113-7D
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DOI：
10.1111/j.1567-1364.2009.00530.x
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发表时间：
2009-08-01
影响因子：
3.2
通讯作者：
Koetter, Peter
中科院分区：
文献类型：
--
作者：
Daran-Lapujade, Pascale;Daran, Jean-Marc;Koetter, Peter
属于CEN. PK家族的酿酒酵母菌株广泛用于基础和应用酵母研究。据报道，这些菌株对钠离子过敏，先前基于微阵列的基因分型研究表明PMR2基因座的非典型组织。在其他S。在酿酒酵母菌株中，该基因座含有1至5个编码质膜钠泵ATP酶的ENA基因。序列分析表明，PMR2基因在猪链球菌中具有较高的同源性。PK113 - 7D揭示了一种新的ENA基因的存在，该基因在核苷酸水平和预测的氨基酸序列水平上与先前描述的ENA基因显示出实质性的序列差异。这种单一的非典型ENA基因的存在与对钠，特别是锂离子的超敏反应相关。天然ENA6基因被钠离子和锂离子转录诱导，但显然，在完全诱导后钠输出的能力不足以达到在其他S.酿酒酵母菌株。然而，CEN.PK菌株的钠和锂超敏性（其在富钠培养基中培养期间是潜在有害的）可以通过ENA6的过表达来抑制。
Saccharomyces cerevisiae strains belonging to the CEN.PK family are widely used in fundamental and applied yeast research. These strains have been reported to be hypersensitive to sodium ions and a previous microarray-based genotyping study indicated an atypical organization of the PMR2 locus. In other S. cerevisiae strains, this locus harbours one to five ENA genes that encode plasma membrane sodium-pumping ATPases. Sequence analysis of the PMR2 locus in S. cerevisiae CEN.PK113-7D revealed the presence of a new ENA gene that showed substantial sequence differences, both at the nucleotide level and at the predicted amino acid sequence level, with previously described ENA genes. The presence of this single and atypical ENA gene correlated with hypersensitivity to sodium and, in particular, to lithium ions. The native ENA6 gene was transcriptionally induced by sodium and lithium ions, but, apparently, the capacity for sodium export upon full induction was insufficient to achieve the levels of sodium and lithium ion tolerance observed in other S. cerevisiae strains. The sodium and lithium hypersensitivity of CEN.PK strains, which is potentially detrimental during cultivation in sodium-rich media, could, however, be suppressed by overexpression of ENA6.