+-r« 
H*UH t i -i 
JB»I 
1 
pMLV-44 — 1 — 1 *■ 
Nucleotide alteration*. Homologou* region* of DNA 
from pMLV-1 and pMLV-48 were »equenced. including the to 
5jfl region re*pon*ible for the difference in inactivity of the two 
clone* of Mo-MLV, The nucleotide numbering tyttem is that used 
by Shinnick et aJ. (22). Base difference* are indicated by circled 
letter*, and the nucleot de number* are *hown. Landmark rettrsc- 
tion endonucleate site* are indicated. Mo-MLV protein coding 
region* are »hown at the top of the figure. 
*' ■ =r 
Z Ml 
£i 3 . .,-L, 
T 
1 
MB 
Fig. 4. The defect responsible for biological Inactivity of pMLV-1 Is an A to 6 
transition at position 1849 In the ga£ gene resulting In an amino acid change 
in the p30 protein from glutamic acid In pMLV-48 to glycine In pMLV-1 and a G 
to C transversion at position 2225 resulting In an amino acid residue change 
from glutamic acid In MLV-48 to aspartic acid in pMLV-1. In the region between 
the end of the gag coding region and the amino terminus of the reverse 
transcriptase coding region (Miller and Verma. 1984). 
Recombinant DNA Research, Volume 1 2 
[ 175 ] 
