Lee Dong-Jik, Bahn Yong-Sun, Kim Hong-Jin, Chung Seung-Yeon, Kang Hyun Ah
From the Department of Life Science, Center for Fungal Pathogenesis, and.
the Department of Biotechnology, Center for Fungal Pathogenesis, Yonsei University, Seoul 120-749, Korea.
J Biol Chem. 2015 Jan 16;290(3):1861-73. doi: 10.1074/jbc.M114.607705. Epub 2014 Dec 4.
Cryptococcus neoformans is an encapsulated basidiomycete causing cryptococcosis in immunocompromised humans. The cell surface mannoproteins of C. neoformans were reported to stimulate the host T-cell response and to be involved in fungal pathogenicity; however, their O-glycan structure is uncharacterized. In this study, we performed a detailed structural analysis of the O-glycans attached to cryptococcal mannoproteins using HPLC combined with exoglycosidase treatment and showed that the major C. neoformans O-glycans were short manno-oligosaccharides that were connected mostly by α1,2-linkages but connected by an α1,6-linkage at the third mannose residue. Comparison of the O-glycan profiles from wild-type and uxs1Δ mutant strains strongly supports the presence of minor O-glycans carrying a xylose residue. Further analyses of C. neoformans mutant strains identified three mannosyltransferase genes involved in O-glycan extensions in the Golgi. C. neoformans KTR3, the only homolog of the Saccharomyces cerevisiae KRE2/MNT1 family genes, was shown to encode an α1,2-mannosyltransferase responsible for the addition of the second mannose residue via an α1,2-linkage to the major O-glycans. C. neoformans HOC1 and HOC3, homologs of the Saccharomyces cerevisiae OCH1 family genes, were shown to encode α1,6-mannosyltransferases that can transfer the third mannose residue, via an α1,6-linkage, to minor O-glycans containing xylose and to major O-glycans without xylose, respectively. Moreover, the C. neoformans ktr3Δ mutant strain, which displayed increased sensitivity to SDS, high salt, and high temperature, showed attenuated virulence in a mouse model of cryptococcosis, suggesting that the extended structure of O-glycans is required for cell integrity and full pathogenicity of C. neoformans.
新型隐球菌是一种有荚膜的担子菌,可在免疫功能低下的人群中引起隐球菌病。据报道,新型隐球菌的细胞表面甘露糖蛋白可刺激宿主T细胞反应并参与真菌致病性;然而,其O-聚糖结构尚未得到表征。在本研究中,我们使用高效液相色谱结合外切糖苷酶处理对附着在隐球菌甘露糖蛋白上的O-聚糖进行了详细的结构分析,结果表明,新型隐球菌的主要O-聚糖是短甘露寡糖,它们大多通过α1,2-连接相连,但在第三个甘露糖残基处通过α1,6-连接相连。野生型和uxs1Δ突变株的O-聚糖谱比较有力地支持了存在带有木糖残基的次要O-聚糖。对新型隐球菌突变株的进一步分析确定了三个参与高尔基体中O-聚糖延伸的甘露糖基转移酶基因。新型隐球菌KTR3是酿酒酵母KRE2/MNT1家族基因的唯一同源物,已证明其编码一种α1,2-甘露糖基转移酶,负责通过α1,2-连接将第二个甘露糖残基添加到主要O-聚糖上。新型隐球菌HOC1和HOC3是酿酒酵母OCH1家族基因的同源物,已证明它们分别编码α1,6-甘露糖基转移酶,可通过α1,6-连接将第三个甘露糖残基转移到含有木糖的次要O-聚糖和不含木糖的主要O-聚糖上。此外,新型隐球菌ktr3Δ突变株对SDS、高盐和高温表现出更高的敏感性,在隐球菌病小鼠模型中显示出毒力减弱,这表明O-聚糖的延伸结构是新型隐球菌细胞完整性和完全致病性所必需的。