The shibire(ts2) mutation of Drosophila melanogaster causes a temperature sensitive inhibition of endocytosis; this in turn leads to synaptic-vesicle depletion and consequent paralysis. Heat-pulses delivered during development of shibire(ts2) individuals affect the morphology of a number of adult structures. A simple screening protocol has been used to isolate several mutations that partially suppress the temperature-sensitive paralytic phenotype of shibire(ts2) mutant animals. All of these mutations very tightly linked to shibire and are likely to be second site intragenic mutations that restore partial activity to the shibire(ts2) product. The mutations suppress both behavioral, and easily-scored developmental phenotypes of shibire(ts2) characterized in this paper. Our results suggest that defects in endocytosis, and not in microtubule interactions, are responsible for all of the phenotypes of shibire(ts2) mutant Drosophila examined in this study.