The Drosophila fliI gene has been determined to affect lipd metabolism and fat storage in the fly. Dmel\fliI is orthologous to the human gene FLII, an action remodeling protein. Classical loss-of-function alleles, RNAi-targeting constructs, and alleles caused by insertional mutagenesis have been generated for Dmel\fliI.
The human FLII gene has not been introduced into flies.
Dmel\fliI primarily participates in cytoskeletal regulation and cell migration as a member of the actin-remodeling protein family. Severe loss-of-function mutations result in larval lethality. Based on studies indicating that fliI modulates the expression of lipogenic enzymes, the effects of fliI mutations on lipid metabolism were assessed. Animals carrying viable loss-of-function fliI mutations are resistant to starvation and have larger amounts of triglycerides in the fat body and intestine; markers of metabolic stress are observed. A fat-body-specific knockdown of fliI results in increased levels of triglycerides; overexpression of fliI significantly reduces the amount of triglycerides. Multiple physical and genetic interactions have been observed for Dmel\fliI; see below and in the fliI gene report.
[updated Feb. 2020 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).
FLII encodes an actin remodeling protein with a gelsolin-like actin binding domain and an N-terminal leucine-rich repeat-protein protein interaction domain. [Gene Cards, FLII; 2020.02.13]
One to one: 1 human to 1 Drosophila.
High-scoring ortholog of human FLII (1 Drosophila to 1 human). Dmel\fliI shares 55% identity and 71% similarity with the human gene.
