The effect of the DSK gastro-peptide on feeding behaviors in Drosophila Melanogaster

By: Christina Mary JosephMentor: Dr. Monica Dus, Ph.DSkirball Institute of BioMedicine, NYU

Laying down the genetics

Laying Down the genetics

Known Behaviors

Sated starved

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Condition

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Food ingestion assay of wildtype flies demonstrate the effect of satiety on ingestion rate

Known Behaviors

Sated starved

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W1118cs food availibilty assay

Condition of flyP

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Food availability assay of wildtype flies demonstrate the effect of satiety on commencement of eating under low availability circumstances

Experiments: PER Assay

Proboscis Extension Reflex Assay. Aids in determining feeding behaviors

Experiments: Ingestion Assay

The ingestion assay aids in determining quantity of food intake.

Experiments: Food availability assay

The food availability assay aids in determining ingestion initiation behaviors

What we found

Figure 1: Percentage of flies that extended their proboscis in both genotypes.

Figure 2: Trends of proboscis extension(TRPA1/DSK- Activated DSK neurons)

What we found

The amount of food eaten by the flies

(1.DSK/KG80- down regulation of DSK 2.DSK/NaChBac- up regulation of DSK)

DSK/+ DSK> kir2.1, tubulingal80ts

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Ingestion assay

Genotypes

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What we found

Food availibility results(1.DSK/KG80- down regulation of DSK2.DSK/NaChBac- up regulation of DSK)

DSK/+ DSK> kir2.1, tubulingal80ts 102039 CCKLR-17D30

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50Food availibility assay: starved

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Conclusion

• The food availability assay showed that starved flies with increased levels of DSK tend to choose not to eat but it did not show starved flies with decreased levels of DSK ate more

• The food ingestion data showed amount eaten by the flies with less DSK ate greater portions than the control while flies with more DSK ate less portions than that of the control

• The PER assay showed that silencing of the DSK neurons led to increased proboscis extension

Discussion

• The data shows strong preliminary promise and a second round of experiments replicating the data shown here will allow us to move into a mammalian model; mice.

• If the data is replicated in the mammalian model, than eating disorders can be prevented by genetic manipulation also thereby preventing long term health defects such as heart disease, kidney failure and even cancer.

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