Taf11, also known as TATA-binding protein-associated factor 11, is involved in multiple biological processes. It is an annotated nuclear transcription factor and plays a role in the assembly of the RNA-induced silencing complex (RLC), enhancing RNAi efficiency [1]. Taf11 also interacts with other transcription-related factors such as TFIIA, and is part of the general transcription factor TFIID complex, which is crucial for RNA polymerase II transcription initiation [3,4].

In Drosophila, taf11 knockout in ovary extract led to defective RLC assembly, and reconstitution of RLC in vitro using recombinant Dcr-2-R2D2 complex, TAF11, and duplex siRNA demonstrated that TAF11 tetramer facilitates Dcr-2-R2D2 tetramerization to enhance siRNA binding and RISC loading activities [1]. In zebrafish, overexpression of TAF11 and taf11 disturbed the migration of cranial neural crest cells and abnormal craniofacial development, as a functionally relevant TAF11 variant affected cell migration via modulating CDH1 and CTNND1, which was associated with the etiology of non-syndromic cleft lip only [2].

In conclusion, Taf11 has important functions in processes like RLC assembly and cell migration. The study of Taf11 using genetic models such as Drosophila and zebrafish has provided insights into its role in RNAi efficiency and craniofacial development-related diseases, helping us better understand its biological significance and potential implications in disease mechanisms.