AI Article Synopsis

  • The malaria vector Anopheles gambiae uses REL2, an NF-kappaB-like transcription factor, to regulate the expression of the antimicrobial peptide Cecropin 1.
  • Through alternative splicing, REL2 produces two protein isoforms: a full-length (REL2-F) and a shorter version (REL2-S), with different roles in immune response against bacteria.
  • REL2-F also plays a role in regulating infection severity by the malaria parasite Plasmodium berghei and is involved in the regulation of at least 10 other immune-related genes.

Article Abstract

We show that, in the malaria vector Anopheles gambiae, expression of Cecropin 1 is regulated by REL2, an NF-kappaB-like transcription factor orthologous to Drosophila Relish. Through alternative splicing, REL2 produces a full-length (REL2-F) and a shorter (REL2-S) protein isoform lacking the inhibitory ankyrin repeats and death domain. RNA interference experiments show that, in contrast to Drosophila Relish, which responds solely to Gram-negative bacteria, the Anopheles REL2-F and REL2-S isoforms are involved in defense against the Gram-positive Staphylococcus aureus and the Gram-negative Escherichia coli bacteria, respectively. REL2-F also regulates the intensity of mosquito infection with the malaria parasite, Plasmodium berghei. The adaptor IMD shares the same activities as REL2-F. Microarray analysis identified 10 additional genes regulated by REL2, including CEC3, GAM1, and LRIM1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1183586PMC
http://dx.doi.org/10.1073/pnas.0504950102DOI Listing

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