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Surprisingly, despite evidence of unregulated activation, Rab7 disease mutants have normal subcellular localization and associate normally with LAMP2 (Fig.  5B) and LysoTracker Red (data not shown).

Figure 3h,i show that mnb mutants have normal exocytosis, as the amount of FM1-43 that unloaded (signal remaining after unloading subtracted from signal from loading) normalized to the amount of loaded was unaltered, thus indicating Mnb reduction causes a specific defect in endocytosis.

bah-1 and bah-2 cuticles are mildly sensitive to alkaline hypochlorite treatment, while bah-3 mutants have normal integrity [16].

A similar regulation of lipid levels is suggested by the finding that disruption of the clock in metabolic tissues decreases triglycerides [15] while clock mutants have normal levels (Fig. 1B).

Although stress-resistant animals are usually long-lived [24] and a raise in chaperone levels is often correlated with increased lifespan [25], [26], we have previously shown that atx-3 mutants have normal lifespan [19].

Additionally, the major circadian output signal of LNvs, PDF, does not appear to be involved in the control of fat body lipids either as Pdf01 mutants have normal triglycerides (Fig. 2E).

This is unexpected, as the AtrabD2b and AtrabD2c single mutants have normal-appearing siliques and seed quantities similar to the wild-type plants.

All mutants had normal number of DD neurons in L1 larvae (data not shown).

The pal1 and pal2 mutants had normal lignin levels, presumably because of gene redundancy.

By contrast, nhsl1b mutants had normal neuroepithelial and floor plate planar polarity (Fig. 5D,F-H).

However, other spl mutants had normal cauline stem lengths (data not shown), while spl15 mutants had slightly stunted stems (Additional file 3) as reported previously [ 13].