Involvement of cryptosporidium parvum Cdg7-FLc-1000 RNA in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3

Zhenping Ming; Ai Yu Gong; Yang Wang; Xin Tian Zhang; Min Li; Nicholas W. Mathy; Juliane K. Strauss-Soukup; Xian Ming Chen

doi:10.1093/infdis/jix392

Involvement of cryptosporidium parvum Cdg7-FLc-1000 RNA in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3

Zhenping Ming, Ai Yu Gong, Yang Wang, Xin Tian Zhang, Min Li, Nicholas W. Mathy, Juliane K. Strauss-Soukup, Xian Ming Chen

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

Intestinal infection by Cryptosporidium parvum causes inhibition of epithelial turnover, but underlying mechanisms are unclear. Previous studies demonstrate that a panel of parasite RNA transcripts of low protein-coding potential are delivered into infected epithelial cells. Using in vitro and in vivo models of intestinal cryptosporidiosis, we report here that host delivery of parasite Cdg7- FLc-1000 RNA results in inhibition of epithelial cell migration through suppression of the gene encoding sphingomyelinase 3 (SMPD3). Delivery of Cdg7-FLc-1000 into infected cells promotes the histone methyltransferase G9a-mediated H3K9 methylation in the SMPD3 locus. Te DNA-binding transcriptional repressor, PR domain zinc fnger protein 1, is required for the assembly of Cdg7-FLc-1000 into the G9a complex and associated with the enrichment of H3K9 methylation at the gene locus. Pathologically, nuclear transfer of Cryptosporidium parvum Cdg7-FLc-1000 RNA is involved in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3.

Original language	English (US)
Pages (from-to)	122-133
Number of pages	12
Journal	Journal of Infectious Diseases
Volume	217
Issue number	1
DOIs	https://doi.org/10.1093/infdis/jix392
State	Published - Jan 1 2018

All Science Journal Classification (ASJC) codes

Immunology and Allergy
Infectious Diseases

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10.1093/infdis/jix392

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Involvement of cryptosporidium parvum Cdg7-FLc-1000 RNA in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3. / Ming, Zhenping; Gong, Ai Yu; Wang, Yang; Zhang, Xin Tian; Li, Min; Mathy, Nicholas W.; Strauss-Soukup, Juliane K.; Chen, Xian Ming.

In: Journal of Infectious Diseases, Vol. 217, No. 1, 01.01.2018, p. 122-133.

Research output: Contribution to journal › Article › peer-review

Ming, Zhenping ; Gong, Ai Yu ; Wang, Yang ; Zhang, Xin Tian ; Li, Min ; Mathy, Nicholas W. ; Strauss-Soukup, Juliane K. ; Chen, Xian Ming. / Involvement of cryptosporidium parvum Cdg7-FLc-1000 RNA in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3. In: Journal of Infectious Diseases. 2018 ; Vol. 217, No. 1. pp. 122-133.

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title = "Involvement of cryptosporidium parvum Cdg7-FLc-1000 RNA in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3",

abstract = "Intestinal infection by Cryptosporidium parvum causes inhibition of epithelial turnover, but underlying mechanisms are unclear. Previous studies demonstrate that a panel of parasite RNA transcripts of low protein-coding potential are delivered into infected epithelial cells. Using in vitro and in vivo models of intestinal cryptosporidiosis, we report here that host delivery of parasite Cdg7- FLc-1000 RNA results in inhibition of epithelial cell migration through suppression of the gene encoding sphingomyelinase 3 (SMPD3). Delivery of Cdg7-FLc-1000 into infected cells promotes the histone methyltransferase G9a-mediated H3K9 methylation in the SMPD3 locus. Te DNA-binding transcriptional repressor, PR domain zinc fnger protein 1, is required for the assembly of Cdg7-FLc-1000 into the G9a complex and associated with the enrichment of H3K9 methylation at the gene locus. Pathologically, nuclear transfer of Cryptosporidium parvum Cdg7-FLc-1000 RNA is involved in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3.",

author = "Zhenping Ming and Gong, {Ai Yu} and Yang Wang and Zhang, {Xin Tian} and Min Li and Mathy, {Nicholas W.} and Strauss-Soukup, {Juliane K.} and Chen, {Xian Ming}",

note = "Funding Information: Financial support. This work was supported by the National Institutes of Health (grant AI116323 to X. M. C.), the Nebraska Stem Cell Research Program (grant LB606 to X. M. C.), and the Nebraska Department of Health and Human Services (LB595 Cancer and Smoking Disease Research Program Development Grant to X. M. C.), the National Center for Research Resources (grant G20RR024001), the China Scholarship Council (to Z. M.), and the National Natural Science Foundation of China (grant 31372194 to Z. M.). Potential conflicts of interest. All authors: No reported conflicts of interest. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.",

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N2 - Intestinal infection by Cryptosporidium parvum causes inhibition of epithelial turnover, but underlying mechanisms are unclear. Previous studies demonstrate that a panel of parasite RNA transcripts of low protein-coding potential are delivered into infected epithelial cells. Using in vitro and in vivo models of intestinal cryptosporidiosis, we report here that host delivery of parasite Cdg7- FLc-1000 RNA results in inhibition of epithelial cell migration through suppression of the gene encoding sphingomyelinase 3 (SMPD3). Delivery of Cdg7-FLc-1000 into infected cells promotes the histone methyltransferase G9a-mediated H3K9 methylation in the SMPD3 locus. Te DNA-binding transcriptional repressor, PR domain zinc fnger protein 1, is required for the assembly of Cdg7-FLc-1000 into the G9a complex and associated with the enrichment of H3K9 methylation at the gene locus. Pathologically, nuclear transfer of Cryptosporidium parvum Cdg7-FLc-1000 RNA is involved in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3.

AB - Intestinal infection by Cryptosporidium parvum causes inhibition of epithelial turnover, but underlying mechanisms are unclear. Previous studies demonstrate that a panel of parasite RNA transcripts of low protein-coding potential are delivered into infected epithelial cells. Using in vitro and in vivo models of intestinal cryptosporidiosis, we report here that host delivery of parasite Cdg7- FLc-1000 RNA results in inhibition of epithelial cell migration through suppression of the gene encoding sphingomyelinase 3 (SMPD3). Delivery of Cdg7-FLc-1000 into infected cells promotes the histone methyltransferase G9a-mediated H3K9 methylation in the SMPD3 locus. Te DNA-binding transcriptional repressor, PR domain zinc fnger protein 1, is required for the assembly of Cdg7-FLc-1000 into the G9a complex and associated with the enrichment of H3K9 methylation at the gene locus. Pathologically, nuclear transfer of Cryptosporidium parvum Cdg7-FLc-1000 RNA is involved in the attenuation of intestinal epithelial cell migration via trans-suppression of host cell SMPD3.

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