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FB2026_01
,
released March 12, 2026
Mutations of the Drosophila gene spen were found to alter larval fat levels in a cell-autonomous manner. Larvae homozygous for a loss-of-function mutation of spen exhibit increased stored fat in fat bodies, but are defective in energy liberation from stores, resulting in starvation sensitivity and major changes in the levels of metabolic enzymes and metabolites. The impact of dietary changes has been studied in this system.
The human ortholog of Dmel\spen is SPEN; the human gene has not been introduced into flies.
[updated Mar. 2021 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).
SPEN encodes a hormone-inducible transcriptional repressor. Repression of transcription by the SPEN product can occur through interactions with other repressors, by the recruitment of proteins involved in histone deacetylation, or through sequestration of transcriptional activators. The SPEN protein contains a carboxy-terminal domain that permits binding to other corepressor proteins. [Gene Cards, SPEN; 2021.03.02]
One to one: 1 human gene to 1 Drosophila gene.
High-scoring ortholog of human SPEN (1 Drosophila to 1 human). Overall, Dmel\spen shares 20% identity and 31% similarity with the human gene, with much higher levels of conservation (>60% identity) within the RRM2_SHARP, RRM3_SHARP, and carboxy-terminal SPOC domains.