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FB2026_01
,
released March 12, 2026
Like MED13, the MED12 protein is a subunit of the Mediator complex. In mice, the MED13 ortholog has been implicated in susceptibility to obesity (pubmed:22541436). There is a single ortholog of MED12 in Drosophila, kto, for which loss-of-function mutations, RNAi-targeting constructs, and alleles caused by insertional mutagenesis have been generated. Dmel\kto is also orthologous to a second very similar gene in human, MED12L.
Neither human gene has been introduced into flies.
Animals homozygous for loss-of-function alleles of Dmel\kto die prior to adulthood, typically during the larval stage. Animals in which RNAi directed against kto is targeted by muscle-specific drivers survive, but exhibit a progressive increase in total triglyceride content; they also exhibit increased resistance to starvation. Knock-down using a heart-specific driver evokes comparable obesity phenotypes. Physical and genetics interactions have been described for Dmel\kto; see below and in the gene report for kto.
[updated Jan. 2018 by FlyBase; FBrf0222196]
The protein products of MED12 and MED12L are subunits of the Mediator complex, a large complex of proteins that functions as a transcriptional coactivator for most RNA polymerase-II-transcribed genes. The MED12 protein is proposed to form a sub-complex with MED13, cyclin C, and CDK8 that can negatively regulate transactivation by mediator. [from Gene Cards, MED12, MED12L; 2017.02.27]
Many to one (2 human to 1 Drosophila); the second human gene is MED12.
Many to one (2 human to 1 Drosophila); the second human gene is MED12L.
High-scoring ortholog of human MED12L and moderate-scoring ortholog of MED12 (1 Drosophila to 2 human). Dmel\kto shares 34-35% identity and 46-48% similarity with the human genes.