Homyk T, Rodriguez A, Weil J
Genetics. 1976 Jul;83(3 PT.2):477-87.
In the course of isolating viable T4 deletions that affect plaque morphology (HOMYK and WEIL 1974), two closely linked point mutant, sip1 and sip2, were obtained. They map between genes t and 52, cause a reduction in plaque size and burst size, and partially suppress the lethality of rII mutants for growth in lambda lysogens. The characteristics demonstrate that sip1 and sip2 are similar to mutants previously reported by FREEDMAN and BRENNER(1972). In addition, D. Hall (personal communication) has shown that sip1 and sip2 are similar to the mutant farP85, which affects the regulation of a number of early genes (Chace and Hall 1975).--Sip suppression of rII mutants can be demonstrated in one-step growth experiments, even when both rII genes are completely deleted. This indicates that sip mutants do not simply reduce the level of rII gene products required for growth in a lambda lysogen. Instead, they alter the growth cycle so as to partially circumvent the need for any rII products.--Mutations at two other sites, designated L1 and L2, reverse the poor phage growth caused by sip and, in the one case tested, reverse the rII-suppressing ability of sip.
在分离影响噬菌斑形态的T4可行缺失的过程中（霍米克和韦尔，1974年），获得了两个紧密连锁的点突变体sip1和sip2。它们定位于基因t和52之间，导致噬菌斑大小和爆发量减小，并部分抑制rII突变体在λ溶原菌中生长的致死性。这些特征表明，sip1和sip2与弗里德曼和布伦纳（1972年）先前报道的突变体相似。此外，D. 霍尔（个人交流）表明，sip1和sip2与突变体farP85相似，后者影响许多早期基因的调控（蔡斯和霍尔，1975年）。——即使rII的两个基因都被完全缺失，在一步生长实验中仍可证明sip对rII突变体的抑制作用。这表明sip突变体并非简单地降低了在λ溶原菌中生长所需的rII基因产物水平。相反，它们改变了生长周期，从而部分规避了对任何rII产物的需求。——另外两个位点L1和L2的突变，可逆转由sip导致的噬菌体生长不良，并且在测试的一个案例中，可逆转sip的rII抑制能力。
