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 journalArticle

6 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)122-133
Number of pages12
JournalJournal of Infectious Diseases
Volume217
Issue number1
DOIs
StatePublished - Jan 1 2018

Fingerprint

Cryptosporidium parvum
Cell Movement
Epithelial Cells
RNA
Methylation
Parasites
Cryptosporidiosis
Sphingomyelin Phosphodiesterase
Genes
Zinc
Proteins
DNA
Infection

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Infectious Diseases

Cite this

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 journalArticle

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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.",
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