The cell walls of fungi are critical for cellular structure and rigidity but also serve as a major communicator to alert the cell to the changing environment. In response to stresses encountered in human hosts, pathogenic fungi remodel their cell walls. Masking the β-1,3-glucan component of the cell wall is critical to escape detection by innate immune cells. We previously demonstrated that β-1,3-glucan is unmasked in response to host temperature stress when translatome reprogramming is defective in Cryptococcus neoformans. Here, we used β-1,3-glucan unmasking as an output to identify signaling modules involved both in masking and in translatome reprogramming in response to host temperature stress. We reveal that the high-osmolarity glycerol (HOG) mitogen-activated protein kinase (MAPK) pathway is involved in translatome reprogramming and that mutants in this pathway display moderate unmasking when grown at 37°C. Additionally, we show that mutants of the cell wall integrity (CWI)/Mpk1 MAPK pathway extensively unmask β-1,3-glucan. While the CWI pathway does not impact translatome reprogramming, our data suggest that it may play a role in the posttranslational regulation of transcription factors that govern masking.

中文翻译：

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葡聚糖揭开识别温度诱导翻译组重编程的调节因子。新型隐球菌

真菌的细胞壁对细胞结构和刚度至关重要，但也是提醒细胞注意不断变化的环境的主要通讯器。为了应对人类宿主中遇到的压力，病原真菌会重塑它们的细胞壁。掩盖细胞壁的 β-1,3-葡聚糖成分对于逃避先天免疫细胞的检测至关重要。我们之前已经证明，当新生隐球菌中的翻译组重编程有缺陷时，β-1,3-葡聚糖会因宿主温度应激而被暴露. 在这里，我们使用 β-1,3-葡聚糖去掩蔽作为输出来识别参与掩蔽和响应宿主温度压力的翻译组重编程的信号模块。我们揭示了高渗透压甘油 (HOG) 丝裂原活化蛋白激酶 (MAPK) 途径参与翻译组重编程，并且该途径中的突变体在 37°C 下生长时显示出适度的暴露。此外，我们表明细胞壁完整性 (CWI)/Mpk1 MAPK 通路的突变体广泛地揭示了 β-1,3-葡聚糖。虽然 CWI 通路不影响翻译组重编程，但我们的数据表明它可能在控制掩蔽的转录因子的翻译后调节中发挥作用。