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. 2006 Dec 20;1(1):e75. doi: 10.1371/journal.pone.0000075

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Milton et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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A threshold trait model was applied the effect of Hsp90 on signalling pathways underlying SC bristle development with assumptions based on current understanding of bristle development and Hsp90 function [26], [46].

The positions of upper and lower thresholds were estimated for P582i and Sami populations, which differed by the presence of wild-type (Sami) or heterozygous mutant (P582i) levels of Hsp90 in otherwise nearly identical genetic backgrounds (N = 450 flies each).

A consistent, but arbitrary, standard deviation (SD) scale was inferred from the frequency of abnormal flies in the P582i background, which had the highest frequencies of abnormal flies.

SC was canalized at 4 over a range of from 5 1/2 to 6 1/2 SD. On the same scale, we estimate that the P582i mutation decreased the strength of proneural and inhibitory bristle development pathways, shifting signalling across the population >2.5 SD to the left relative to fixed upper and lower thresholds.