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首页> 外文期刊>Antimicrobial agents and chemotherapy. >Aspergillus fumigatus Afssn3-Afssn8 Pair Reverse Regulates Azole Resistance by Conferring Extracellular Polysaccharide, Sphingolipid Pathway Intermediates, and Efflux Pumps to Biofilm
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Aspergillus fumigatus Afssn3-Afssn8 Pair Reverse Regulates Azole Resistance by Conferring Extracellular Polysaccharide, Sphingolipid Pathway Intermediates, and Efflux Pumps to Biofilm

机译：Aspergillus fumigatus afssn3-afssn8对通过赋予细胞外多糖，鞘脂途径中间体和流出泵至生物膜来逆转抗唑抗性

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Antifungal treatment is often ineffectual, partly because of biofilm formation. In this study, by using a combined forward and reverse genetic strategy, we identified that nucleus-localized AfSsn3 and its partner AfSsn8, which constitute a Cdk8-cyclin pair, are required for azole resistance in Aspergillus fumigatus. Deletion of Afssn3 led to increased absorption and utilization of glucose and amino acids. Interestingly, absorption and utilization of glucose accelerated the extracellular polysaccharide formation, while utilization of the amino acids serine, threonine, and glycine increased sphingolipid pathway intermediate accumulation. In addition, the absence of Afssn3 induced the activity of the efflux pump proteins. These factors indicate the mature biofilm is responsible for the major mechanisms of A. fumigatus resistance to azoles in the Delta Afssn3 mutant. Collectively, the loss of Afssn3 led to two "barrier" layers between the intracellular and extracellular spaces, which consequently decreased drug penetration into the cell.
机译：抗真菌治疗通常是无效的，部分是因为生物膜形成。在本研究中，通过使用组合的前进和逆向遗传策略，我们鉴定了构成CDK8-Cyclin对的核局部AFSSN3及其合作伙伴AFSSN8是在Aspergillus fumigatus中的唑抗性所必需的。缺失AFSSN3导致葡萄糖和氨基酸的吸收和利用率增加。有趣的是，葡萄糖的吸收和利用加速了细胞外多糖的形成，而氨基酸丝氨酸，苏氨酸和甘氨酸的利用增加了鞘脂途径中间积累。此外，没有AFSSN3诱导出鼻泵蛋白的活性。这些因素表明成熟的生物膜负责A.Fumigatus抗唑类AFSSN3突变体中氮的主要机制。统称，AFSSN3的损失导致细胞内和细胞外空间之间的两个“屏障”层，从而降低了细胞中的药物渗透。

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