Mark S. Carter

TL;DR: In this paper, the authors performed sequence analysis of reverse transcriptase-polymerase chain reaction products from fetal and adult thymus and found that newly transcribed T-cell receptor-β pre-mRNAs (intron-bearing) are frequently derived from ptc-bearing genes but such transcripts rarely accumulate as mature (fully spliced) TCR-β transcripts.

TL;DR: The results suggest that nonsense codon recognition may occur in the nucleus, as well as examining the molecular mechanism for this putative nuclear response by using the T‐cell receptor‐beta gene, which acquires PTCs as a result of programmed rearrangements that occur during normal thymic ontogeny.

TL;DR: It is shown that the T cell receptor–β (TCRβ) gene gives rise to an alternatively spliced transcript that skips the offending mutations that generate such nonsense codons, and this alt-mRNA is up-regulated by a transfer RNA–dependent scanning mechanism that responds specifically to mutations that disrupt the reading frame.

TL;DR: An unusual spliced intron from the constant region of the T cell receptor-beta (TCR-beta) locus is described that is relatively stable in mammalian cells and accumulates as a set of lariat RNA structures in the nucleus of T cells.

TL;DR: A repressional mechanism involving a labile repressor protein may be responsible for the inhibition of RNA splicing since treatment of SL12.4 cells with the protein synthesis inhibitor cycloheximide reversibly induces a rapid and dramatic accumulation of fully spliced T CR-beta transcripts in the cytoplasm, concomitant with a decline in TCR-beta pre-mRNAs in the nucleus.