Abstract
Heme oxygenase (HO) is a ubiquitous enzyme responsible for heme breakdown, which yields carbon monoxide (CO), biliverdin (BV) and ferrous ion. Here we show that the Aedes aegypti heme oxygenase gene (AeHO – AAEL008136) is expressed in different developmental stages and tissues. AeHO expression increases after a blood meal in the midgut, and its maximal transcription levels overlaps with the maximal rate of the further modified A. aegypti biglutaminyl-biliverdin (AeBV) pigment production. HO is a classical component of stress response in eukaryotic cells, being activated under oxidative stress or increased heme levels. Indeed, the final product of HO activity in the mosquito midgut, AeBV, exerts a protective antioxidant activity. AeHO, however, does not seem to be under a classical redox-sensitive transcriptional regulation, being unresponsive to heme itself, and even down regulated when insects face a pro-oxidant insult. In contrast, AeHO gene expression responds to nutrient sensing mechanisms, through the target of rapamycin (TOR) pathway. This unusual transcriptional control of AeHO, together with the antioxidant properties of AeBV, suggests that heme degradation by HO, in addition to its important role in protection of Aedes aegypti against heme exposure, also acts as a digestive feature, being an essential adaptation to blood feeding.
Highlights
Aedes aegypti is a vector of important human viral diseases such as yellow fever and dengue, and more recently has been associated with the large-scale emergence of viruses such as Chikungunya[1] and Zika[2]
One Heme oxygenase (HO)-1 predicted ortholog was found in the A. aegypti genome (VectorBase Genome Assembly: AaegL5), suggesting that this mosquito expresses only one isoform of HO
Since aegypti heme oxygenase (AeHO) in not canonically regulated, yet it is still induced throughout blood digestion, we investigated whether a nutrient sensor – such as the kinase Target of Rapamycin (TOR) – mechanism would be involved
Summary
Aedes aegypti is a vector of important human viral diseases such as yellow fever and dengue, and more recently has been associated with the large-scale emergence of viruses such as Chikungunya[1] and Zika[2] Both adult males and females feed on nectar, but only females require the ingestion of large amounts of vertebrate blood, as a nutritional source for oogenesis. The heme degradation pathway has only been described in the mosquito A. aegypti[9] and in the hemipteran Rhodnius prolixus[10], vector of Chagas disease. In both cases heme degradation process displays several peculiarities when compared to vertebrates pathway. The physiological relevance of HO and of its product BV IX as antioxidant components and the regulation of HO expression in the context of adaptation to hematophagy have not been investigated so far
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