V(D)J recombination occurs imprecisely, so that while transcripts from both alleles are expressed, only one is able to give rise to a functional surface antigen receptor.
[7] The feedback inhibition model is similar to the asynchronous recombination mode, but it emphasizes the mechanisms that maintain the rearrangement asynchrony.
[10] The allelic exclusion of light chain genes Igκ and Igλ is a process that is controlled by the monoallelic initiation of V(D)J recombination.
While little is known about the mechanism leading to the allelic exclusion of Igλ genes, the Igκ locus is generally inactivated by RAG-mediated deletion of the exon Cκ.
While this feedback mechanism is mainly achieved through inhibition of the juxtaposition of V and D-J segments, the down-regulation of transcription and suppression of RAG accessibility also plays a role.
[13][14][15][16] In mice vomeronasal sensory neurons, an odorant receptor coding sequence's exogenous transcription from a V1R promoter can stop endogenous V1R genes from being transcribed.
[14][15][16][19][20] GATA3 transgenic overexpression by a 2.5- to 5-fold increase partly due to Gata3 transcriptional activation from monoallelic to biallelic primarily resulted in both alleles of TCR𝛽 recombining.
[14] V𝛽 Recombination signal sequences (RSSs) with poor qualities suppressed one allele's expression of two TCR𝛽 genes.
[21] Low quality V𝛽 recombinase targets randomly constrain two functional rearrangements’ production which imposes TCR𝛽 allelic exclusion.