Tait R C, Kado C I, Rodriguez R L
Mol Gen Genet. 1983;192(1-2):32-8. doi: 10.1007/BF00327643.
The plasmid pOri3 is a derivative of the origin of replication of pSa. Replication is defective as a result of a truncated repA gene, the product of which is required for plasmid replication. The defective replication is complemented by the presence of the intact repA gene of pSa, or by the presence of the plasmid R6K. The basis of this complementation has been examined by comparing the nucleotide sequence of the origin of pSa with that of R6K. A 13 base pair sequence present twice in the origin of pSa has homology with a 13 base pair sequence that is present fourteen times in the origin of R6K. These sequences may be the binding sites for the initiator proteins of these two plasmids. The location of these binding sites relative to the genes for the initiator proteins suggests that an autoregulatory control mechanism for the synthesis of the initiator proteins may also play a role in the control of plasmid copy number.
质粒pOri3是pSa复制起点的衍生物。由于repA基因截短，其复制存在缺陷，而该基因产物是质粒复制所必需的。pSa完整的repA基因的存在，或质粒R6K的存在可弥补这种有缺陷的复制。通过比较pSa和R6K复制起点的核苷酸序列，研究了这种互补作用的基础。在pSa复制起点中出现两次的13个碱基对序列，与在R6K复制起点中出现14次的13个碱基对序列具有同源性。这些序列可能是这两种质粒引发蛋白的结合位点。这些结合位点相对于引发蛋白基因的位置表明，引发蛋白合成的自动调节控制机制可能也在质粒拷贝数的控制中发挥作用。
