Which of the following mutations would promote malignancy in cells whose proliferation is inhibited by TGFβ?

a. overexpression of Smad2               

b. loss of Smad 4

c. overexpression of TGFβ receptor I

d. loss of TGFβ receptor II

Wild type E. coli metabolizes the sugar lactose by expressing the enzyme ß-galactosidase. You have isolated a mutant that you call lac1–, which cannot synthesize ß-galactosidase and cannot grow on lactose (Lac–). During an condition isolate a mutation that constitutively expresses abnormally high levels of ßgalactosidase, which you designate lacc. Preliminary P1 transduction experiments indicate that lacc  is linked to the Tn5 insertion.  To map lacc  relative to lac1– you set up two reciprocal crosses. In the first cross you grow P1 on a strain that carries the Tn5 insertion and the lac1– mutation. You then use this lysate to infect a lacc mutant and select for Kanr. From 100 Kanr transductants examined, 20 are Lac–, 76 express ß-galactosidase constitutively and 4 show normal ß-galactosidase expression. In the second cross you grow P1 on a strain that carries the Tn5 insertion and the lacc mutation. You then use this lysate to infect a lac1– mutant, and select for Kanr. From 100 Kanr transductants examined, 81 are Lac– and 19  express ß-galactosidase constitutively. So what will be the correct order of  the Tn5 insertion and the lac1– and lacc  mutations. Express any measured distances as cotransduction frequencies.