Disease relevance of TRG@

• The absolute number of trans-rearrangements between the TCRG and TCRB loci is predictive of lymphoma risk: a severe combined immune deficiency (SCID) murine model [1].
• Comparison between adult and pediatric T-ALL patients did not show any obvious differences in TCRG gene configuration [2].
• T cell receptor gamma (TCRG) gene rearrangements in T cell acute lymphoblastic leukemia refelct 'end-stage' recombinations: implications for minimal residual disease monitoring [2].
• The high frequency, easy detectability, rare oligoclonality, and frequent 'end-stage' recombinations make TCRG gene rearrangements principal targets for PCR-based detection of minimal residual disease (MRD) in T-ALL [2].
• Based on restriction fragments, the TRG rearrangements can be assigned to given V and J segments, in normal T-cells, T leukemias and lymphomas [3].

High impact information on TRG@

• The interleukin 7 receptor is required for T cell receptor gamma locus accessibility to the V(D)J recombinase [4].
• T cell rearranging gene gamma (TRG gamma) and T cell antigen receptor beta (TCR beta) chain gene rearrangement and transcription were studied in a series of patients with B-lineage acute lymphoblastic leukemia (ALL), in which the Ig H chain genes are rearranged and the surface phenotype reproduces the stages of normal pre-B maturation [5].
• Furthermore, evidence of TCR-beta and/or TRG-gamma gene rearrangement was observed in four AML, all of which belonged to the Igh-rearranged TdT+ group [6].
• We also show that in B-lineage ALL, the cells probably use the same V gamma genes for TRG gamma rearrangements as the malignant cells in T-ALL and the polyclonal T cells [5].
• The correlations between surface phenotype, rearrangement of TRG gamma, TCR beta, and Ig H chain genes were analyzed [5].

Biological context of TRG@

• The clonal TCRB, TCRG and TCRD gene rearrangements were analyzed for gene segment usage and for the size and composition of their junctional regions [7].
• Moreover, we analyze the TCRG haplotypes in four different populations (French, Lebanese, Tunisian, and Black African) to underline their interest for population genetics [8].
• Only TRG1@ is included within a region of homology with human TRG locus on chromosome 7, thus TRG2@ locus appears to be peculiar to ruminants [9].
• We have identified such negative cis-acting sequences in the 3' non-coding region of the human TcR gamma (TRG) locus, upstream of an enhancer located at 6.5 kb of the TcR C gamma 2 gene (TRGC2) [10].
• Altogether, 83% of TCRG gene rearrangements involved either the most upstream Vgamma2 gene (including four cases with interstitial deletion of 170 bp in Vgamma2) and/or the most downstream Jgamma2.3 segment, which can be perceived as 'end-stage' recombinations [2].

Anatomical context of TRG@

• The human T-cell receptor gamma (TRG) genes [11].
• TCRG and TCRB mRNAs were expressed in the cells of precursor T- but not B-cell leukemia patients studied [12].
• On Southern blot analysis, the mature T-cell leukemia cells studied had rearranged TCRG and TCRB while IGHJ remained as in the germ line [12].
• Trans-rearrangements between TCRG and TCRD loci, similar in structure and frequency to those observed previously in human lymphoid tissues, were demonstrated in normal mouse thymus by PCR with crossed V gamma/J delta and V delta/J gamma primer pairs [13].
• A total of 54 primers was developed (1) to amplify rearrangements of the TCRD, TCRG, and IGK (Kde) genes as well as TAL1 deletions; (2) to sequence the junctional regions and breakpoint fusion regions; and (3) to perform MRD detection in bone marrow or peripheral blood samples during follow-up of ALL patients [14].

Associations of TRG@ with chemical compounds

• The RR was 1.67 for allele C1 at TCRA1, 3.35 for allele D2 at TCRA2, 1.66 for allele B2 at TCRG, and 1.35 for allele B at TCRB, showing no significant association [15].
• METHODS: We used polymerase chain reaction (PCR) for amplification of junctional region of rearranged IgH, TCRD and TCRG genes in combination with heteroduplex analysis in polyacrylamide gel [16].
• It had been assumed that this cDNA, termed TRG for tunicamycin resistance gene, encoded GPT enzyme [17].
• Our studies provide an explanation for a previous observation that TCRG mRNA levels, but not mRNA levels for T cell receptor alpha and -beta, are increased by ionomycin treatment [18].
• Monoclonal B cells were detected by studying rearrangement patterns of the hypervariable CDR III regions within the immunoglobulin heavy chain gene locus and the T-cell receptor gamma chain gene (TCRG) [19].

Regulatory relationships of TRG@

• The simultaneous results on the TRG2@ locus molecular organization in sheep and on the phylogenetic analysis of cattle and sheep V expressed sequences indicate that at least six TRG clusters distributed in the two loci are present in these ruminant animals [9].

Other interactions of TRG@

• In the human T cell receptor gamma (TRG) locus, fourteen variable (TRGV) genes belonging to four subgroups have been identified upstream of two constant region (TRGC) genes [20].
• Rearrangements to the JP1, JP and JP2 segments in the human T-cell rearranging gamma gene (TRG gamma) locus [21].
• Using Southern blotting and the polymerase chain reaction, two of 60 TCRG coding joints were abnormal [22].
• Evolution of TRG clusters in cattle and sheep genomes as drawn from the structural analysis of the ovine TRG2@ locus [9].
• Thirteen clones reactive with anti-TigammaA were tested; it was found that the second TRG allele (i.e., the one which does not involve V9-JP) of these cells was either in germ-line configuration or, more frequently, rearranged with a downstream V gamma gene joined to a J segment of the TRG1 region [23].

Analytical, diagnostic and therapeutic context of TRG@

• Clonality assessment through Southern blot (SB) analysis of TCRB genes or polymerase chain reaction (PCR) analysis of TCRG genes is important for diagnosing suspect mature T-cell proliferations [24].
• To determine the sensitivity of heteroduplex analysis with renaturation at 4 degrees C, (c)DNA of T cell malignancies with proven clonal rearrangements was serially diluted in (c)DNA of polyclonal mononuclear peripheral blood cells and amplified using V and C primers (TCRB genes) or V and J primers (TCRG and TCRD genes) [25].
• We cloned 200 kb of the rabbit TRG locus and determined the TRGV gene usage in adult and newborn rabbits by RT-PCR [26].
• These results show the validity and reliability of the fluorescent PCR method for routine detection of IGH, TCRG and TCRD rearrangements [27].
• Results from site-directed mutations and electrophoretic mobility shift assays strongly suggest that this sequence mediates the ionomycin-induced activation of the TCRG enhancer [18].

References