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Extremely alkaline intracellular pH in the anterior stomach of larval yellow fever mosquitoes ( Aedes aegypti )
Author(s) -
Onken Horst,
Parks Scott K,
Goss Greg G,
Moffett David F
Publication year - 2008
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.22.1_supplement.759.4
Subject(s) - aedes aegypti , intracellular ph , stomach , lumen (anatomy) , apical membrane , chemistry , intracellular , biophysics , biology , biochemistry , anatomy , larva , microbiology and biotechnology , ecology , membrane
The anterior stomach of larval Aedes aegypti is an alkalinizing organ where basolateral V‐ATPase drives luminal alkalinization to a pH of up to 12. However, the apical mechanisms involved are unknown. We hypothesized that luminal alkalinization involves absorption of H + via apical H + channels. Such a system would require increased intracellular pH (pH i ) to function effectively. pH i was monitored using live cell imaging and BCECF as a pH‐dependent fluorophore. Serotonin (0.2 ìM), which stimulates luminal alkalinization, increased pH i in the anterior stomach from 7.0 ± 0.1 to 7.7 ± 0.1 (N = 64), whereas pH i was not affected in the posterior stomach (6.7 ± 0.1 before and 6.8 ± 0.1 after serotonin; N = 19). Perfusing the lumen with pH 10 saline increased pH i to 8.6 ± 0.1 (N = 41), suggesting a marked apical H + permeability. However, in presence of luminal Zn 2+ (10 ìM) similarly high pH i values were recorded (8.2 ± 0.1; N = 15), indicating that an apical proton channel, if present at all, cannot be blocked with Zn 2+ . The rate of pH change after switching to pH 10 in the lumen in the presence or absence of luminal Zn 2+ was also not different. Together these results show that remarkably alkaline pH i values can be observed in the anterior stomach of larval Aedes aegypti . However, further investigation is required to determine the transporters involved in this unique physiological system. This work was supported by NIH (1R01AI063463‐01A2).