It seems that loss or gain of cato function causes neuronal defects. Like cato , embryos mutant for pros show neuronal defects, although the basis of these defects is not known. It was asked whether cato expression depends on pros function. In situ hybridization to mRNA in whole-mount embryos reveals that cato is expressed dynamically during neurogenesis and is confined to the developing PNS .
Expression is switched off as cells begin to undergo terminal differentiation.
Double-labelling experiments using antibodies to Ato in conjunction with a Cato RNA probe confirm that the onset of cato expression correlates with the refinement of Ato expression to isolated SOPs. In PNS cells other than the chordotonal SOPs, cato expression appears delayed relative to SOP formation. Although subsequent SOP formation is dynamic and individual SOPs are difficult to follow, this delay seems to hold true for other external sense organ cells too. Interestingly, the difference in timing of expression between cato and Ase appears reversed in chordotonal SOP formation. Expression of cato appears to continue in the progeny of many or all SOPs during late stage 11 and early stage 12 and at this point resembles the pattern of ase .