July 7, 2019  |  

Genome analysis of three Pneumocystis species reveals adaptation mechanisms to life exclusively in mammalian hosts.

Authors: Ma, Liang and Chen, Zehua and Huang, Da Wei and Kutty, Geetha and Ishihara, Mayumi and Wang, Honghui and Abouelleil, Amr and Bishop, Lisa and Davey, Emma and Deng, Rebecca and Deng, Xilong and Fan, Lin and Fantoni, Giovanna and Fitzgerald, Michael and Gogineni, Emile and Goldberg, Jonathan M and Handley, Grace and Hu, Xiaojun and Huber, Charles and Jiao, Xiaoli and Jones, Kristine and Levin, Joshua Z and Liu, Yueqin and Macdonald, Pendexter and Melnikov, Alexandre and Raley, Castle and Sassi, Monica and Sherman, Brad T and Song, Xiaohong and Sykes, Sean and Tran, Bao and Walsh, Laura and Xia, Yun and Yang, Jun and Young, Sarah and Zeng, Qiandong and Zheng, Xin and Stephens, Robert and Nusbaum, Chad and Birren, Bruce W and Azadi, Parastoo and Lempicki, Richard A and Cuomo, Christina A and Kovacs, Joseph A

Pneumocystis jirovecii is a major cause of life-threatening pneumonia in immunosuppressed patients including transplant recipients and those with HIV/AIDS, yet surprisingly little is known about the biology of this fungal pathogen. Here we report near complete genome assemblies for three Pneumocystis species that infect humans, rats and mice. Pneumocystis genomes are highly compact relative to other fungi, with substantial reductions of ribosomal RNA genes, transporters, transcription factors and many metabolic pathways, but contain expansions of surface proteins, especially a unique and complex surface glycoprotein superfamily, as well as proteases and RNA processing proteins. Unexpectedly, the key fungal cell wall components chitin and outer chain N-mannans are absent, based on genome content and experimental validation. Our findings suggest that Pneumocystis has developed unique mechanisms of adaptation to life exclusively in mammalian hosts, including dependence on the lungs for gas and nutrients and highly efficient strategies to escape both host innate and acquired immune defenses.

Journal: Nature communications
DOI: 10.1038/ncomms10740
Year: 2016

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