  \textit{Vibrio harveyi} and \textit{Vibrio cholerae} have quorum sensing
pathways with similar design and highly homologous components including
multiple small RNAs (sRNAs). However, the associated luminescence phenotypes of
strains with sRNA deletions differ dramatically: in \textit{V. harveyi}, the
sRNAs act additively; however, in \textit{V. cholerae}, the sRNAs act
redundantly. Furthermore, there are striking differences in the luminescence
phenotypes for different pathway mutants in \textit{V. harveyi} and \textit{V.
cholerae}. However these differences have not been connected with the observed
differences for the sRNA deletion strains in these bacteria. In this work, we
present a model for quorum sensing induced luminescence phenotypes focusing on
the interactions of multiple sRNAs with target mRNA. Within our model, we find
that one key parameter -- the fold-change in protein concentration necessary
for luminescence activation -- can control whether the sRNAs appear to act
additively or redundantly. For specific parameter choices, we find that
differences in this key parameter can also explain hitherto unconnected
luminescence phenotypes differences for various pathway mutants in \textit{V.
harveyi} and \textit{V. cholerae}. The model can thus provide a unifying
explanation for observed differences in luminescence phenotypes and can also be
used to make testable predictions for future experiments.
