Role of the iron mobilization and oxidative stress regulons in the genomic response of yeast to hydroxyurea

Role of the iron mobilization and oxidative stress regulons in the genomic response of yeast to hydroxyurea
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DOI:
10.1007/s00438-005-0077-5
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发表时间:
2006-02-01
影响因子:
3.1
通讯作者:
Mann, C
Mann, C
中科院分区:
生物学3区
文献类型:
--
作者:
Dubacq, C;Chevalier, A;Mann, C

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羟基脲(HU)是核糖核苷酸还原酶的特异性抑制剂,因此损害dNTP合成和DNA复制。酵母细胞的长期转录反应,以羟基脲进行了研究,使用DNA微阵列包含所有酵母编码序列。我们发现,氧化还原反应的雅普调节子和铁动员的Aft调节子在用HU处理的酵母细胞中被激活。Yap 1在细胞核中积累响应HU,但HU激活的雅普调节子仅部分依赖于Yap 1和Yap 1 δ突变体对HU不过敏。相反,AFT 1和AFT 2转录因子基因的缺失阻断了HU激活的一个子集的Aft调节子和aft1 Δ aft2 Δ双突变体是超敏的铁抑制的方式HU。这些结果突出了氧化还原和铁动员调节子在细胞对HU的反应中的重要性。
Hydroxyurea (HU) is a specific inhibitor of ribonucleotide reductase and thus impairs dNTP synthesis and DNA replication. The long-term transcriptional response of yeast cells to hydroxyurea was investigated using DNA microarrays containing all yeast coding sequences. We show that the redox-responsive Yap regulon and the iron-mobilization Aft regulon are activated in yeast cells treated with HU. Yap1 accumulates in the nucleus in response to HU, but HU activation of the Yap regulon was only partially dependent on Yap1 and yap1 Delta mutants were not hypersensitive to HU. In contrast, deletion of the AFT1 and AFT2 transcription factor genes blocked the HU activation of a subset of the Aft regulon and the aft1 Delta aft2 Delta double mutant was hypersensitive to HU in an iron-suppressible manner. These results highlight the importance of the redox and iron mobilization regulons in the cellular response to HU.