Description

The loss of autophagy function in the motor cortex has been associated with progression of neurodegenerative symptoms in Parkinson’s disease (Kaila and Lang 2015; Fahn et al. 2004). To analyze possible effects of the bec-1(ok691) mutation on neuronal density, we followed the transgene juIs76 as it produced GFP marked D-type motor neurons (Figure 1 A-C). Previous research has found lineage timing of GABAergic (VD) motor neuron differentiation in C. elegans to occur before animals reach adulthood (Jin et al., 1994). These studies show a delay in development of ventral D-type motor neurons in bec-1(ok691) homozygous mutants (Figure 1 D). Maturation and development of VD motor neurons to the levels of controls were seen on day 5 of adulthood in bec-1(ok691) homozygous mutants. However, our discovery in delayed lineage timing of VD motor neurons suggests a potential role of BEC-1 in neurodevelopment. This is consistent with findings in mouse models, where ortholog Beclin 1 plays an essential role in cell differentiation during development (Cecconi and Levine, 2008). Instead of observing rapid neurodegeneration of VD motor neurons, resulting from the bec-1(ok691) mutation, we observed a rapid decrease in lifespan (Ashley and Holgado, 2019) as VD motor neurons were differentiated. This conclusion should be considered as preliminary as we have not verified by an alternative line of investigation (e.g., a second allele or transgene rescue) that the observed phenotypes are specific to bec-1(ok691).There is additional evidence that suggests autophagy’s role in mechanisms of cell editing in early developmental stages of C. elegans (Di Bartolomeo et al., 2010).