Non-Classical Gluconeogenesis-Dependent Glucose Metabolism in

43 Annual Meeting of SBBq
Foz do Iguaçu, PR, Brazil, 2014
Non-Classical Gluconeogenesis-Dependent Glucose Metabolism in
Rhipicephalus microplus Embryonic Cell Line BME26
Renato Martins1, Bárbara Pitta1, Leonardo Abreu, Jorge Moraes2, Helga Gomes2,
Itabajara da Silva Vaz Jr3, Carlos Logullo1.
1
LQFPP and UEA-RJ, UENF; Rio de Janeiro, Brazil. 2 Nupem UFRJ Macaé. 3
Universidade Federal do Rio Grande do Sul (UFRGS)
Introduction: The release of acaricides into the environment and the
development of tick acaricide resistance are some of these problems. Many areas
have achieved progress in recent years in order to replace classical control methods,
using the vaccination and the application of biocontrol agents. Nevertheless, despite
the acquisition of molecular information has increased recently, the comprehensive
understanding of molecular mechanisms, including the energy metabolism
regulation, which aid on the identification of potential antigens for improved vaccines
are still incomplete. Methods: we evaluated several genes involved in
gluconeogenesis, glycolysis and glycogen metabolism, the major pathways for
carbohydrate catabolism and anabolism, in the BME26 Rhipicephalus microplus
embryonic cell line after glucose treatment. Control cells (cells maintained with
glucose 80mM); Low-glucose cells (cell maintained without glucose) and HighGlucose cells (cells maintained with glucose 160mM). Results: The results indicate
that several genes, such as glycogen synthase (GS), glycogen synthase kinase 3
(GSK3), phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase
(G6Pase), displayed mutual gene regulation in response to glucose treatment.
Surprisingly, the transcription of gluconeogenic enzymes was found to increase
alongside that of glycolytic enzymes, especially pyruvate kinase, under high glucose
treatment. In addition, RNAi data from this study revealed that the transcription of
gluconeogenic genes in BME26 cells is controlled by GSK-3. Conclusion:
Collectively, these results improve our understanding of how glucose metabolism is
regulated at the genetic level in tick cells.
Palavra chave: Metabolism, Tick, Cell
Patrocínio: FAPESP, CNPq and CAPES