Jofuku K D, Schipper R D, Goldberg R B
Department of Biology, University of California, Los Angeles 90024-1606.
Plant Cell. 1989 Apr;1(4):427-35. doi: 10.1105/tpc.1.4.427.
We investigated the molecular basis of a soybean Kunitz trypsin inhibitor (KTi) gene mutation that prevents the accumulation of Kunitz trypsin inhibitor protein during seed development. We found that mRNA encoding the major Kunitz trypsin inhibitor protein (KTi3 mRNA) is reduced at least 100-fold in null (KTi-) embryos but that KTi3 gene transcriptional activity is similar in Kunitz trypsin inhibitor producing embryos (KTi+) and in KTi- embryos. We sequenced the Kunitz trypsin inhibitor KTi3 gene from both KTi3+ and KTi3- lines and found that these genes differ by only three nucleotides (+481, +486, and +487) within the KTi3 coding region. Alteration of these nucleotides results in a frameshift within the KTi3- gene that causes premature termination during translation. Our results suggest that the KTi3- frameshift mutation results in KTi3- mRNA destabilization and leads to a drastic reduction in KTi3 mRNA prevalence.
我们研究了大豆Kunitz胰蛋白酶抑制剂（KTi）基因突变的分子基础，该突变阻止了Kunitz胰蛋白酶抑制剂蛋白在种子发育过程中的积累。我们发现，在无（KTi-）胚胎中，编码主要Kunitz胰蛋白酶抑制剂蛋白的mRNA（KTi3 mRNA）减少了至少100倍，但KTi3基因的转录活性在产生Kunitz胰蛋白酶抑制剂的胚胎（KTi+）和KTi-胚胎中相似。我们对来自KTi3+和KTi3-品系的Kunitz胰蛋白酶抑制剂KTi3基因进行了测序，发现这些基因在KTi3编码区内仅相差三个核苷酸（+481、+486和+487）。这些核苷酸的改变导致KTi3-基因内的移码，从而在翻译过程中导致提前终止。我们的结果表明，KTi3-移码突变导致KTi3- mRNA不稳定，并导致KTi3 mRNA丰度急剧降低。
