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CLONING OF A TRYPSIN‐LIKE SERINE PROTEASE AND EXPRESSION PATTERNS DURING P LASMODIUM FALCIPARUM INVASION IN THE MOSQUITO, A NOPHELES DIRUS ( P EYTON AND H ARRISON)
Author(s) -
Sriwichai Patchara,
Rongsiryam Yupha,
Jariyapan Narissara,
Sattabongkot Jetsumon,
Apiwathnasorn Chamnarn,
Nacapunchai Duangporn,
Paskewitz Susan
Publication year - 2012
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.21034
Subject(s) - biology , midgut , serine protease , plasmodium falciparum , parasite hosting , anopheles , malaria , complementary dna , protease , blood meal , virology , cloning (programming) , gene , innate immune system , plasmodium (life cycle) , hemolymph , microbiology and biotechnology , genetics , immunology , immune system , biochemistry , enzyme , zoology , botany , larva , world wide web , programming language , computer science
Understanding specific gene regulation during responses to malaria infection is key to dissecting the mosquito defense mechanisms and host/parasite interactions. A full‐length serine protease c DNA was isolated from the fat body of female Anopheles dirus , a major malaria vector in T hailand. The predicted amino acid sequence of SERF 4 identifies it as a member of the serine protease family containing a single trypsin‐like protease domain. Digestive trypsins function in the female mosquito midgut and are inducible in two phases in this tissue upon blood intake. However, the gene was highly upregulated in the midgut at day 3 postinfection by Plasmodium falciparum . In situ hybridization confirmed that SERF 4 transcripts were located in the midgut epithelial cells rather than hemocytes or other tissues associated with the midgut. SERF 4 was also strongly downregulated in the whole insects at day 16 after infection in comparison with the blood‐fed control. Changes in the expression of the SERF 4 gene in response to infection with this human malaria parasite suggest a role in parasite‐specific innate immunity.