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. 2015 Sep 24;11(9):e1005513. doi: 10.1371/journal.pgen.1005513

Fig 1. Flies with impaired kinin or CAMB signaling show significant defects in the ecdysis FAP.

Fig 1

(A) Roles for kinin in the ecdysis behavioral sequence were investigated by analysis of behavioral defects in kinin cell-killing (CK) flies and homozygous piggyBac-insertional kinin receptor mutant flies (Lkr f02594 / Lkr f02594). In both instances, pre-ecdysis durations were highly variable. Precise flip-out of piggyBac insertion by piggyBac transposase rescued normal pre-ecdysis behavior. Complementation testing with a kinin-receptor-gene deficient line [Df(3L)Exel6105] also showed high variation in pre-ecdysis duration. The small black arrowheads represent pre-ecdysis durations of individual animals. Error-bars represent standard deviation (SD). (B) Relative expression ratio of kinin receptor genes in control and homozygous Lkr f02594. Kinin receptor mutant Lkr f02594 showed significant reduction (26.2%) in gene expression level. Error-bars represent standard error of mean (SEM) (* P < 0.01; Student’s t-test). (C) EGFP staining patterns of kinin and CAMB (Pburs-Gal4) neurons. (D) Flies bearing targeted cell-killing (CK) of CAMB neurons exhibit prolonged pre-ecdysis and complete absence of ecdysis and post-ecdysis. Pre-ecdysis behavior begins with the normal frequency of rhythmic contractions, but the behavior weakens gradually after 10 min, ending at ~26 min. Error-bars represent standard deviation (SD).