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首页> 外文期刊>Molecular and Cellular Biology >The Cryptococcus neoformans Rim101 Transcription Factor Directly Regulates Genes Required for Adaptation to the Host
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The Cryptococcus neoformans Rim101 Transcription Factor Directly Regulates Genes Required for Adaptation to the Host

机译：新型隐球菌Rim101转录因子直接调节适应宿主所需的基因

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The Rim101 protein is a conserved pH-responsive transcription factor that mediates important interactions between several fungal pathogens and the infected host. In the human fungal pathogen Cryptococcus neoformans, the Rim101 protein retains conserved functions to allow the microorganism to respond to changes in pH and other host stresses. This coordinated cellular response enables this fungus to effectively evade the host immune response. Preliminary studies suggest that this conserved transcription factor is uniquely regulated in C. neoformans both by the canonical pH-sensing pathway and by the cyclic AMP (cAMP)/protein kinase A (PKA) pathway. Here we present comparative transcriptional data that demonstrate a strong concordance between the downstream effectors of PKA and Rim101. To define Rim101-dependent gene expression during a murine lung infection, we used nanoString profiling of lung tissue infected with a wild-type or rim101Δ mutant strain. In this setting, we demonstrated that Rim101 controls the expression of multiple cell wall-biosynthetic genes, likely explaining the enhanced immunogenicity of the rim101Δ mutant. Despite its divergent upstream regulation, the C. neoformans Rim101 protein recognizes a conserved DNA binding motif. Using these data, we identified direct targets of this transcription factor, including genes involved in cell wall regulation. Therefore, the Rim101 protein directly controls cell wall changes required for the adaptation of C. neoformans to its host environment. Moreover, we propose that integration of the cAMP/PKA and pH-sensing pathways allows C. neoformans to respond to a broad range of host-specific signals.
机译：Rim101蛋白是一种保守的pH响应转录因子，可介导几种真菌病原体与被感染宿主之间的重要相互作用。在人类真菌病原体新隐球菌中，Rim101蛋白保留了保守的功能，使微生物能够响应pH值和其他宿主压力的变化。这种协调的细胞反应使这种真菌能够有效逃避宿主的免疫反应。初步研究表明，这种保守的转录因子在新孢梭菌中均受规范的pH传感途径和环AMP（cAMP）/蛋白激酶A（PKA）途径的唯一调节。在这里，我们介绍比较转录数据，证明PKA和Rim101的下游效应子之间有很强的一致性。为了定义鼠肺部感染期间Rim101依赖性基因的表达，我们使用了用野生型或 rim101 Δ突变株感染的肺组织的nanoString分析。在这种情况下，我们证明Rim101控制多个细胞壁生物合成基因的表达，这可能解释了 rim101 Δ突变体的增强的免疫原性。尽管其上游调控有差异，但新孢梭菌Rim101蛋白仍能识别保守的DNA结合基序。利用这些数据，我们确定了该转录因子的直接靶标，包括参与细胞壁调控的基因。因此，Rim101蛋白直接控制新孢子虫适应宿主环境所需的细胞壁变化。此外，我们建议整合cAMP / PKA和pH敏感途径可以使新孢梭菌对多种宿主特异性信号作出反应。

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