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Fig. 9 | Molecular Neurodegeneration

Fig. 9

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. 9

N-terminal tau fragments (wild-type or with A152T mutation) are not toxic to C. elegans neurons. a Bar diagram depicts the N-terminal fragment of tau (amino acids Met1-Leu243) derived from full-length Tau. The pan-neuronal snb-1 promoter drives the expression of wild-type N-t- or mutant N-t-fragment (Tauwt-Nt and TauAT-Nt respectively) in C. elegans neurons. b Blot showing the protein expression levels in worms carrying N-terminal fragments or full-length tau transgenes as extrachromosomal arrays. 30 synchronized day-1 old adult worms from each transgene (Ex[Tauwt-Nt], Ex[TauAT-Nt], Ex[Tauwt] and Ex[TauAT]) were lysed and subjected to western blot analysis using N-terminal Tau specific DA9 antibody (epitope at aa 100-130). Non-tg worms serve as control and tubulin as loading control. c Age-related comparison of rate of body thrashing in liquid for days 1, 5 and 7 from the respective transgenic animals. In contrast to full-length tau (Tauwt or TauAT), expression of N-terminal Tau fragments in C. elegans neurons (Tauwt-Nt or TauAT-Nt) cause only slight reductions (~10-13 %) in thrashing at day 1 and day 5. The data points represent the mean (±SEM) thrashing rate and time point, n ≥ 30. Two-way ANOVA followed by Bonferroni correction was used for multiple comparisons. d Immunostaining of animals expressing either wild-type- or mutant-N-t tau fragments at different time points with N-terminal tau-specific antibody SA4473. Top panels depict nerve ring ganglion while the bottom panels show nerve cords. N-terminal Tau fragments show localization restricted to cell bodies and nuclei (white arrows), as nerve processes are largely invisible, in contrast to the situation with full-length Tau (see Fig. 1c)

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