In a large-scale screen for obesity susceptibility genes in Drosophila, a number of candidate genes proved to be members of or regulators of the hedgehog signaling pathway. RNAi-effected knockdown of these genes specifically in fat body (but not in neurons, muscle, or oenoctyes) results in significant changes in measured triglyceride levels. Genes identified include the hedgehog ligand (hh), the binding protein ihog, the coreceptor smoothened (smo), the coactivator nejire (nej), the downstream transcription factor cubits interuptus (ci), the hedgehog target and positive regulator Sxl, and the negative regulator Su(fu).
See also the FlyBase report for the Hedgehog Signaling Pathway (FBgg0000978).
[updated Jan. 2019 by FlyBase; FBrf0222196]
Obesity is an abnormal accumulation of body fat, usually 20% or more over an individual's ideal body weight. Obesity is associated with increased risk of illness, disability, and death. (http://medical-dictionary.thefreedictionary.com/obesity).
The development of obesity is recognized as having both genetic and environmental components (https://www.sciencelearn.org.nz/resources/203-obesity-genetic-or-environmental).
High-scoring ortholog of human SHH, DHH, and IHH (3 human to 1 Drosophila).
Moderate-scoring ortholog of human BOC and CDON (2 human to 2 Drosophila); the other Drosophila gene is boi.
High-scoring ortholog of human SMO (1 human to 1 Drosophila).
High-scoring ortholog of human EP300 and CREBBP (2 human to 1 Drosophila).
High-scoring ortholog of human GLI3 and GLI2; moderate-scoring ortholog of GLI1 (3 human to 1 Drosophila).
Low-scoring ortholog of human RBMS1, RBMS2, RBMS3; the Drosophila gene shep is more closely related to all 3 human genes.
High-scoring ortholog of human SUFU (1 human to 1 Drosophila).