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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Tau mutant A152T, a risk factor for FTD/PSP, induces neuronal dysfunction and reduced lifespan independently of aggregation in a C. elegans Tauopathy model

Fig. 2

Mutant TauAT leads to substantial damage in GABAergic motor neurons. Punc-25::gfp reporter that labels GABAergic inhibitory neurons with GFP, was crossed with respective tau-transgenic worms to visualize these neurons. a Cartoon depicting the GABAergic inhibitory motor system in an adult worm. b-f depict representative maximum intensity projections (MIP) of day-1 old adults of the transgenes. For whole worm MIPs, see Additional file 11. Abnormalities seen as gaps in the GABAergic inhibitory neurons are highlighted by arrowheads. GABAergic neurons show normal connectivity in non-tg reporter worms, both dorsal and ventral nerve cords are intact (b). Expression of Tauwt produces dose dependent abnormalities in GABAergic neurons, with Tauwt -hi neurons (d) accumulating more damage than Tauwt -lo (c). However, mutant TauAT expression leads to severe abnormalities in the form of gaps in the dorsal and ventral nerve cords, both TauAT-lo (e) and TauAT-hi (f). One of the striking features of mutant TauAT worms is the absence of stretches of dorsal cord (bracketed areas), not found in non-tg worms or Tauwt worms. See TableĀ 1 for detailed quantitative analysis

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