%0 Journal Article
%T Germ band retraction as a landmark in glucose metabolism during Aedes aegypti embryogenesis
%A Wagner Vital
%A Gustavo Rezende
%A Leonardo Abreu
%A Jorge Moraes
%A Francisco JA Lemos
%A Itabajara Vaz
%A Carlos Logullo
%J BMC Developmental Biology
%D 2010
%I BioMed Central
%R 10.1186/1471-213x-10-25
%X Glucose metabolism was investigated throughout Aedes aegypti (Diptera) embryonic development. Both cellular blastoderm formation (CBf, 5 h after egg laying - HAE) and germ band retraction (GBr, 24 HAE) may be considered landmarks regarding glucose 6-phosphate (G6P) destination. We observed high levels of glucose 6-phosphate dehydrogenase (G6PDH) activity at the very beginning of embryogenesis, which nevertheless decreased up to 5 HAE. This activity is correlated with the need for nucleotide precursors generated by the pentose phosphate pathway (PPP), of which G6PDH is the key enzyme. We suggest the synchronism of egg metabolism with carbohydrate distribution based on the decreasing levels of phosphoenolpyruvate carboxykinase (PEPCK) activity and on the elevation observed in protein content up to 24 HAE. Concomitantly, increasing levels of hexokinase (HK) and pyruvate kinase (PK) activity were observed, and PEPCK reached a peak around 48 HAE. Glycogen synthase kinase (GSK3) activity was also monitored and shown to be inversely correlated with glycogen distribution during embryogenesis.The results herein support the hypothesis that glucose metabolic fate changes according to developmental embryonic stages. Germ band retraction is a moment that was characterized as a landmark in glucose metabolism during Aedes aegypti embryogenesis. Furthermore, the results also suggest a role for GSK3 in glycogen balance/distribution during morphological modifications.The mosquito Aedes aegypti is vector of urban yellow fever and also the main dengue vector [1]. One of the major problems involving dengue transmission is that A. aegypti embryos enter dormancy at the end of embryogenesis, surviving and remaining viable for several months inside the egg [2-4]. This extended viability is possible due to the acquisition of embryonic desiccation resistance, a biological mechanism that is believed to involve the formation and maturation of serosal cuticle, a layer covering the embryo [5]. De
%U http://www.biomedcentral.com/1471-213X/10/25