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Vault RNA expression in Leishmania‐exposed macrophages
Author(s) -
Farrow Anitra Leanette,
Misra Smita,
Chaudhuri Gautam
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a80-d
Subject(s) - leishmania , rna , biology , vault (architecture) , gene , gene expression , leishmania major , transcription (linguistics) , microbiology and biotechnology , genetics , parasite hosting , structural engineering , world wide web , computer science , engineering , linguistics , philosophy
Leishmaniasis is a parasitic disease that affects scores of people in the tropical world. The causative agent for this often‐fatal human disease is the protozoan of the genus Leishmania . Others and we have recently shown that these parasites manipulate the expressions of several genes in their host macrophages at the time of infection to their benefit to establish infection. One of the genes that are down regulated in the macrophages upon exposure to Leishmania is the SRP RNA, which is the RNA component of the signal recognition particle (SRP) (JBC, 275 :19428‐19432, 2000; JBC, 280 :29364‐29373, 2005). The transcription of the SRP RNA is affected. Since SRP RNA is transcribed by RNA polymerase III from a type 4 promoter, our hypothesis is that all the genes that have the type 4 pol III promoter are affected by the exposure to Leishmania . Besides the SRP RNA gene, the only other mammalian gene that is transcribed from such promoter is that of the vault RNA. We report here our preliminary studies on the expressions of different variants of vault RNAs in the control and the Leishmania ‐exposed macrophages. Vault is the largest known ribonucleoprotein particle known in the mammalian cells and is known to aid in the regulation of cell growth. Regulation of vault RNA by Leishmania in macrophages thus reveals a unique strategy by the parasite to renovate its host cell environment to make the cell more hospitable for its living and propagation. Supported by NIH grants 5‐R01AI42327‐03, 2S06GM08037‐24, and 3SO6GM008037‐33S1 to GC.