These results rule out the role of endocytosis as an explanation for the defects in clu mutants.
A plausible explanation for the defects in cerebellar foliation of the PEX13 brain mutants is the impaired migration of granule cells and abnormal Purkinje cell development.
There are two possible explanations for the defect of aho-3(nj15) mutants: starved aho-3(nj15) mutants always seek out 23 °C regardless of their cultivation temperature or just higher temperatures.
The identification of immediate targets for individual cryptococcal Pmt proteins may provide further explanations for the defects in pathogenicity found for the pmt1 and pmt4 mutants of C. neoformans.
There are several possible explanations for the defects in transcriptional fidelity observed here.
One possible explanation for the initiation defect of TNT/Gr68a males could be that they have a problem in the visual system which prevents them from locating the female.
An alternative explanation for the locomotion defect is that since APP is expressed throughout the brain in this mouse, it might contribute to deficits in the brain motor centers.
One possible explanation for the virulence defect is that ssn8 mutant cells may have difficulty in crossing the blood brain barrier due to their elongated cell morphology, or may be defective in putative brain predilection factor(s), which is yet to be demonstrated.
One potential explanation for the observed defect in IFNγ secretion was that factors present or absent in the septic milieu might reversibly impair cytokine secretion.
