Age-dependent motility defects and neurodegeneration in <i>alfa-1(ok3062)</i> mutants.

<div><p>(A) <i>alfa-1(ok3062)</i> mutants showed motility defects leading to paralysis of 60% of the population by day 12 of adulthood compared to 20% for N2 worms (P<0.0001).</p> <p>(B) <i>alfa-1(ok3062)</i> worms are more sensitive to aldicarb-induced paralysis than N2 worms (P<0.0001).</p> <p>(C) Percentage of wild type N2 or <i>alfa-1(ok3062)</i> worms displaying a swimming-induced paralysis phenotype after 8 hours in liquid culture (** P<0.001).</p> <p>(D) Example of gap (indicated by arrow) along a neuronal process in animals expressing the <i>unc-47p::GFP</i> reporter.</p> <p>(E) Quantification of neurodegeneration at day 9 of adulthood associated with <i>alfa-1(ok3062)</i> in different neuronal populations including cholinergic neurons marked by <i>unc-17p::GFP</i>, dopaminergic neurons visualized with <i>dat-1p::GFP</i>, or GABAergic neurons revealed by <i>unc-47p::GFP</i>. Significant neurodegeneration was observed in the GABAergic neurons of <i>alfa-1(ok3062)</i> mutants (**P<0.001).</p>