Developmental Genetics 
overt phenotype. However, further analysis of the 
fyn mutation has revealed that thymocytes are un- 
able to proliferate in response to stimulation 
through the T cell receptor, demonstrating that 
this kinase is essential for normal thymocyte 
function. Surprisingly, peripheral T cells can re- 
spond through the T cell receptor, implying that 
-Other kinase (s) may be involved. This mutation 
may have further effects on the repertoire of T 
cells, and further studies are under way. 
To test the concept that 5rc-related kinases 
compensate for one another, we have crossbred 
the mutant mice and examined progeny for dou- 
ble mutant genotypes. The vast majority of src- 
yes and src-fyn double mutants die at birth — 
supporting the compensation hypothesis. The 
nature of the defect in the double mutants is 
under further investigation. This second aspect of 
our research has been supported in part by the 
National Institutes of Health. 
Expression pattern of the ^galactosidase (^-gal) gene in blastocysts of a 'promoter trap" strain 
of transgenic mice, showing labeling (blue) in both the inner cell mass and the outlying trophec- 
toderm. By this technique, mice derived from selected embryonic stem cells can be used both to 
trace the activity of a ^-gal-tagged gene and to mutate the strain. 
Research of Glenn Friedrich and Philippe Soriano. 
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