tion for its product, perhaps the first such function 
to be ascribed to a Qa gene. 
Dr. Geliebter is also Assistant Professor and 
Head of Laboratory at the Rockefeller University. 
Books and Chapters of Books 
Joyce, S., Garrett, T.P.J., Geliebter, J., Sun, R., and 
Nathenson, S.G. 1991. Structural correlates of 
MHC class I restricted antigen specific and allo- 
reactive immunity. In Processing and Presenta- 
tion of Antigens (McCIuskey, J., Ed.). Boca Ra- 
ton, FL: CRC Press, pp 109-130. 
Article 
Pfaflfenbach, G.M., Uehara, H., Geliebter J., Nath- 
enson, S.G., and Schulze, D.H. 1991. Analysis of 
the H-2 K*""^ mutant: correlation of structure with 
function. Mol Immunol 28:697-701. 
TRANSLATION 
Raymond F. Gesteland, Ph.D., Investigator 
Ribosome Hopping 
Dr. Gesteland's laboratory has characterized the 
determinants in mRNA of Escherichia coli phage 
T4's gene 60 that allow ribosomes to bypass effi- 
ciently a 50-nucleotide coding gap, and studies are 
under way to explore this unusual biochemical 
mechanism. A genetic approach has been to look for 
bacterial mutants that restore hopping efficiency to 
mutants of gene 60 that are defective in the mRNA 
signals for hopping. 
One mutation is a single amino acid substitution 
in ribosomal protein L9. This change restores hop- 
ping to constructs that are deficient in a stem struc- 
ture located at the beginning of the gap sequences. 
Somehow the altered L9 can compensate for the lack 
of a particular structure in the mRNA. Little is 
known about the role that L9 normally plays in the 
ribosome. This new mutant should provide a useful 
tool for understanding both hopping and ribosomes. 
A second mutant that restores hopping to many 
defects in the 60 mRNA (including altered amino 
acid sequences in the growing peptide chain) is, 
surprisingly, in the gene for lipoamide dehydroge- 
nase. This defect in the TCA cycle results in an ATP 
deficit that elicits the stringent response and the syn- 
thesis of ppGpp, which somehow alters ribosome 
fidelity or kinetics to give the enhanced hopping 
phenotype. 
The role of the 15-amino acid peptide is being 
studied by systematic mutagenesis. Sequential re- 
placement of each residue with aspartic acid 
showed that many sites have a modest influence on 
hopping, and a few seem crucially important. Fur- 
ther constructs will guide biochemical experiments 
to elucidate the role of the peptide in hopping. 
Messenger RNA Stability 
A series of Shine-Dalgarno (SD) and initiation co- 
don changes show that SD efficiency but not initia- 
tion codon strength is necessary for lacZ mRNA sta- 
bility in E. coli. However, a point mutant in the 
fourth codon of lacZ is shown to affect translation 
initiation and, consequently, mRNA stability. The 
point mutant exerts its effect on translation initia- 
tion by creating an occluding secondary structure 
partly within the translation initiation region. The 
extent of the secondary structure and a putative 
stem-loop are investigated by gene fusion and site- 
directed mutagenesis. The secondary structure is 
shown to be contained within codons 1-23 of the 
lacZ transcript. 
Readthrough 
The gag and pol genes of Moloney murine leuke- 
mia virus (Mo-MuLV) are separated by an in-frame 
UAG codon. Translational readthrough of this stop 
codon allows synthesis of a gag-pol fusion polypep- 
tide, the sole source of pol gene products. In vitro 
translation studies have shown that readthrough of 
the UAG codon is dependent on a 3' pseudoknot that 
is separated from the UAG codon by an 8-nt purine- 
rich spacer. 
Comparison of the Mo-MuLV pseudoknot se- 
quence with other viruses that utilize stop codon 
readthrough shows the potential for pseudoknot 
formation in several of these viruses, a similar 
purine-rich sequence immediately 3' to the UAG co- 
don and a group of conserved nucleotides in the 
second loop of the pseudoknot. Several of these 
viral pseudoknot sequences have been tested and 
GENETICS 195 
