Alternative titles; symbols
HGNC Approved Gene Symbol: BTG1
Cytogenetic location: 12q21.33 Genomic coordinates (GRCh38): 12:92,140,278-92,145,846 (from NCBI)
Rimokh et al. (1991) cloned the breakpoint of a t(8;12) chromosomal translocation in a case of B-cell chronic lymphocytic leukemia and isolated a coding sequence mapping to chromosome 12q22. This sequence detected a 1.8-kb transcript in virtually all tissues tested except in the brain and muscle where the signal was barely detectable. The putative gene corresponding to this sequence, termed BTG1 for B-cell translocation gene 1, was shown to be highly conserved in evolution; a similar 1.8-kb transcript could be detected in murine and chicken tissue by using a human BTG1 DNA probe.
Rouault et al. (1992) established the genomic organization of the BTG1 gene. The full-length cDNA isolated from a lymphoblastoid cell line contained an open reading frame of 171 amino acids. BTG1 expression was maximal in the G0/G1 phases of the cell cycle and downregulated when cells progressed throughout G1. Furthermore, transfection experiments using NIH 3T3 cells indicated that BTG1 negatively regulates cell proliferation. Rouault et al. (1992) postulated that BTG1 is a member of a new family of antiproliferative genes.
Bakker et al. (2004) found increased Foxo3a (602681) expression during differentiation in a mouse erythroid progenitor cell line, and DNA microscreens identified Btg1 (109580) as a novel Foxo3a target. Ectopic expression of Btg1 inhibited the expansion of mouse erythroid progenitor cells, which was dependent on the protein arginine methyltransferase-1 (HRMT1L2; 602950)-binding domain of Btg1. Bakker et al. (2004) concluded that the modulation of protein-arginine methylation activity by BTG1 may be a FOX-dependent mechanism regulating erythroid differentiation.
Hwang et al. (2020) identified BTG1 and BTG2 (601597) as factors responsible for T-cell quiescence. BTG1/2-deficient T cells show an increased proliferation and spontaneous activation due to a global increase in mRNA abundance, which reduces the threshold to activation. BTG1/2 deficiency leads to an increase in polyadenylate tail length, resulting in a greater mRNA half-life. Thus, BTG1 and BTG2 promote the deadenylation and degradation of mRNA to secure T-cell quiescence. Hwang et al. (2020) concluded that their study revealed a key mechanism underlying T-cell quiescence and suggested that low mRNA abundance is a crucial feature for maintaining quiescence.
Rimokh et al. (1991) identified the BTG1 gene on chromosome 12q22, at the breakpoint of a t(8;12) chromosomal translocation.
Stumpf (2020) mapped the BTG1 gene to chromosome 12q21.33 based on an alignment of the BTG1 sequence (GenBank BC064953) with the genomic sequence (GRCh38).
Bakker, W. J., Blazquez-Domingo, M., Kolbus, A., Besooyen, J., Steinlein, P., Beug, H., Coffer, P. J., Lowenberg, B., van Lindern, M., van Dijk, T. B. FoxO3a regulates erythroid differentiation and induces BTG1, an activator of protein arginine methyl transferase 1. J. Cell Biol. 164: 175-184, 2004. [PubMed: 14734530] [Full Text: https://doi.org/10.1083/jcb.200307056]
Hwang, S. S., Lim, J., Yu, Z., Kong, P., Sefik, E., Xu, H., Harman, C. C. D., Kim, L. K., Lee, G. R., Li, H.-B., Flavell, R. A. mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence. Science 367: 1255-1260, 2020. [PubMed: 32165587] [Full Text: https://doi.org/10.1126/science.aax0194]
Rimokh, R., Rouault, J. P., Wahbi, K., Gadoux, M., Lafage, M., Archimbaud, E., Charrin, C., Gentilhomme, O., Germain, D., Samarut, J., Magaud, J. P. A chromosome 12 coding region is juxtaposed to the MYC protooncogene locus in a t(8;12)(q24;q22) translocation in a case of B-cell chronic lymphocytic leukemia. Genes Chromosomes Cancer 3: 24-36, 1991. [PubMed: 2069907] [Full Text: https://doi.org/10.1002/gcc.2870030106]
Rouault, J.-P., Rimokh, R., Tessa, C., Paranhos, G., Ffrench, M., Duret, L., Garoccio, M., Germain, D., Samarut, J., Magaud, J.-P. BTG1, a member of a new family of antiproliferative genes. EMBO J. 11: 1663-1670, 1992. [PubMed: 1373383] [Full Text: https://doi.org/10.1002/j.1460-2075.1992.tb05213.x]
Stumpf, A. M. Personal Communication. Baltimore, Md. 09/16/2020.