The fruit flie, Drosophila melanogaster
A snapshot of dFOXO ChIP-Seq in Genome Browser
A typical survival curve
Immunostaining of insulin-like peptides (DILPs)
reduced insulin/IGF-1 signaling prolongs life span in Drosophila?
Reduced insulin/IGF-1 signaling increases the life span of
nematodes, flies and rodents. However the underlying molecular mechanisms of
this robust effect remain unclear. Genetic evidence places forkhead transcription factor FoxO
as the downstream effector of insulin/IGF-1
signaling. Thus, insulin signaling through its control of FoxO is a potentially universal system to regulate aging.
A critical goal at this time is to identify the proximal targets of insulin/FoxO signaling that orchestrate these mechanisms of
To identify downstream effectors involved in insulin-mediated
life span in Drosophila
2. Lifespan analysis
The red flour beetle, Tribolium castaneum
G protein-coupled receptor (GPCRs)
Effects on insect development by RNAi targeting bursicon receptor
Large-scale RNAi screen of G protein-coupled receptors (GPCRs) in the red flour beetle, Tribolium castaneum
G protein-coupled receptors (GPCRs) belong to the largest superfamily of integral cell membrane proteins and play crucial roles in physiological processes including behavior, development and reproduction. Because of their broad and diverse roles in cellular signaling, GPCRs are the therapeutic targets for many prescription drugs. However, there is no commercial pesticide targeting insect GPCRs.
In this study, I employed functional genomics methods and used the red flour beetle, Tribolium castaneum, as a model system to study the physiological roles of GPCRs during the larval growth, molting and metamorphosis.
1. To identify all non-sensory GPCRs inTribolium genome
2. Apply RNAi screen to study the physiological roles of identified GPCRs
Life cycle the yellow fever mosquito, Aedes aegypti. Application of methoprene blocks the transition from pupae to adults.
TUNEL assay was used to monitor cell death occuring at the midgut remodeling.
regulation of midgut remodeling during metamorphsis of the yellow fever mosquito, Aedes aegypti
The Yellow Fever Mosquito, Aedes aegypti, is historically the primary vector for the
viruses that cause human dengue and yellow fever. Methoprene, as a juvenile
hormone (JH) analogue, has been used for almost 30 years as the primary
insecticide to control the mosquito. However the mode of action of methoprene
is poorly characterized.
This project is focused on the molecular mechanism of methoprene during midgut remodeling of A. aegypti. Knowledge gained from this study will be useful for development of novel strategy for mosquito control and slowing down the
development of methoprene-resistance of mosquito population.
1. To uncover the underlying mechanisms through which methoprene blocks the transition from pupae to mosquito adults
2. To study the role of methoprenesis on ecdysone-mediated metamorphosis in mosquitoes