DOI: 10.1093/jisesa/ieag119 ISSN: 1536-2442

Molecular and functional characterization of a typical 2-Cys peroxiredoxin and its developmental and pyriproxyfen-responsive expression in Aedes albopictus (Diptera: Culicidae)

Batuhan Askim Arslanhan, Samba Deguene Diop, Simge Sahin, Ahsen Meliha Toroslu, Alina Denis Kizgin, Gokmen Zafer Pekmezci, Abdullah Inci, Alparslan Yildirim

Abstract

The Asian tiger mosquito, Aedes albopictus (Skuse, 1894) (Diptera: Culicidae), is established and expanding across the Black Sea region, but the redox processes associated with its development and response to insect growth regulators remain poorly understood. We characterized a typical 2-Cys peroxiredoxin (Prx2) by examining intraspecific sequence variation, conserved protein features, enzymatic activity, developmental transcription, and transcription following exposure to 0.06 ppb pyriproxyfen. The coding region was polymorphic among Turkish isolates, but all substitutions were synonymous, and the deduced amino acid sequence was conserved. Catalytic cysteines and hallmark motifs supported classification as a typical 2-Cys peroxiredoxin. Recombinant His-tagged Prx2 migrated at the expected molecular size and removed hydrogen peroxide in a concentration- and thiol-dependent manner. Basal transcript abundance varied across development, reaching its lowest level in pupae and higher levels in adults. Exposure to 0.06 ppb pyriproxyfen was associated with increased Prx2 transcript abundance in L3 and L4 larvae, whereas no statistically detectable treatment-related difference was observed among the surviving pupae or adults at the sampled time points. Together, these findings identify Prx2 as a conserved, functional thiol peroxidase and demonstrate a pyriproxyfen-associated larval transcriptional response under the conditions tested. Because this concentration was not independently validated as sublethal in the present colony and later-stage sampling necessarily comprised survivors of the original exposure, the data do not distinguish developmental attenuation of the response from survivor selection.

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