Silent information regulator 2 proteins encoded by Cryptosporidium parasites
| Autor: | Hiro Yasukawa, Kenji Yagita |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Sequence analysis
Molecular Sequence Data Protozoan Proteins Cryptosporidium Dictyostelium discoideum Green fluorescent protein parasitic diseases Animals Humans Sirtuins Dictyostelium Amino Acid Sequence Gene Peptide sequence Cellular localization Cell Nucleus Cryptosporidium parvum Genetics General Veterinary biology Sequence Analysis DNA General Medicine DNA Protozoan biology.organism_classification Molecular biology Infectious Diseases Microscopy Fluorescence Insect Science Parasitology Cryptosporidium hominis Polymorphism Restriction Fragment Length |
| Zdroj: | Parasitology Research. 107:707-712 |
| ISSN: | 1432-1955 0932-0113 |
| DOI: | 10.1007/s00436-010-1925-8 |
| Popis: | Screening in a database has revealed that Cryptosporidium hominis encodes a silent information regulator 2 (Sir2), a nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase. Cellular localization of the protein, ChSir2, was analyzed by the use of the social amoeba Dictyostelium discoideum as a model system. Fluorescent microscopic analysis showed that ChSir2 fused with green fluorescent protein was localized in the D. discoideum nucleus. D. discoideum expressing ChSir2 grew faster and reached higher cell density than did D. discoideum harboring a control vector. These results suggest that ChSir2 is a nucleus-localizing protein that plays an important role in the growth of C. hominis. We cloned and sequenced the genes for Sir2 orthologs encoded by three isolates of C. hominis, two isolates of Cryptosporidium parvum and one isolate of Cryptosporidium meleagridis. The orthologs conserve critical catalytic or NAD-binding residues but do not have similarity with human Sir2 proteins (SIRTs). Cryptosporidium Sir2 orthologs would therefore be attractive therapeutic targets. The Cryptosporidium orthologs were classified into four variants based on their nucleotide sequences. Each of the four variants produces its own unique restriction fragment length polymorphism pattern by digestion with TfiI. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink