Goff S A, Cone K C, Fromm M E
U.S. Department of Agriculture/University of California, Berkeley, Albany 94710.
Genes Dev. 1991 Feb;5(2):298-309. doi: 10.1101/gad.5.2.298.
Genes encoding fusions between the maize regulatory protein C1 and the yeast transcriptional activator GAL4 and mutant C1 proteins were assayed for their ability to trans-activate anthocyanin biosynthetic genes in intact maize tissues. The putative DNA-binding region of C1 fused to the transcriptional activation domain of GAL4 activated transcription of anthocyanin structural gene promoters in c1 aleurones, c1 Rscm2 embryos, and c1 r embryogenic callus. Cells receiving these constructs accumulated purple anthocyanin pigments. The C1 acidic region fused to the GAL4 DNA-binding domain activated transcription of a GAL4-regulated promoter. An internal deletion of C1 also induced pigmentation; however, frameshifts in either the amino-terminal basic or carboxy-terminal acidic region blocked trans-activation, and the latter generated a dominant inhibitory protein. Fusion constructs between the wild-type C1 cDNA and the dominant inhibitor allele C1-I cDNA were used to identify the amino acid changes in C1 responsible for the C1-I inhibitory phenotype. Results from these studies establish that amino acids within the myb-homologous domain are critical for transcriptional activation.
对编码玉米调节蛋白C1与酵母转录激活因子GAL4融合体以及突变C1蛋白的基因,检测了它们在完整玉米组织中反式激活花青素生物合成基因的能力。与GAL4转录激活结构域融合的C1推定DNA结合区域,在c1糊粉层、c1 Rscm2胚以及c1 r胚性愈伤组织中激活了花青素结构基因启动子的转录。接受这些构建体的细胞积累了紫色花青素色素。与GAL4 DNA结合结构域融合的C1酸性区域激活了GAL4调控启动子的转录。C1的内部缺失也诱导了色素沉着;然而,氨基末端碱性区域或羧基末端酸性区域的移码突变均阻断了反式激活,并且后者产生了一种显性抑制蛋白。野生型C1 cDNA与显性抑制等位基因C1-I cDNA之间的融合构建体,用于鉴定C1中导致C1-I抑制表型的氨基酸变化。这些研究结果表明,myb同源结构域内的氨基酸对于转录激活至关重要。