Bronner C E, Welker D L, Deering R A
Department of Molecular and Cell Biology, Pennsylvania State University, University Park 16802.
Genetics. 1988 Dec;120(4):959-64. doi: 10.1093/genetics/120.4.959.
The tmpA600 mutation confers thymidylate synthase deficiency and thymidine auxotrophy to Dictyostelium discoideum. The tdrA600 mutation enhances transport of thymidine and thereby reduces the auxotrophic requirement of tmpA600 strains. The tmpA locus maps to linkage group III. The tdrA600 mutation is dominant and cosegregates with both linkage groups IV and VI, possibly because of a translocation between the two. The tdrA600 allele is sufficient to allow efficient incorporation of exogenous [3H]thymidine or [3H]uridine into TCA-precipitable material and to sensitize the cell to the nucleoside-analog inhibitor, 5-fluorodeoxyuridine. These properties make the tdrA mutation useful for studies requiring labelling of DNA or RNA in vivo.
tmpA600突变赋予盘基网柄菌胸苷酸合成酶缺陷和胸苷营养缺陷型。tdrA600突变增强了胸苷的转运，从而降低了tmpA600菌株的营养缺陷需求。tmpA基因座定位于连锁群III。tdrA600突变是显性的，并且与连锁群IV和VI共分离，这可能是由于两者之间的易位。tdrA600等位基因足以使外源性[3H]胸苷或[3H]尿苷有效地掺入三羧酸循环沉淀物质中，并使细胞对核苷类似物抑制剂5-氟脱氧尿苷敏感。这些特性使得tdrA突变对于需要在体内标记DNA或RNA的研究很有用。
