Macroautophagy (hereon referred as Autophagy) is a cellular housekeeping mechanism that uses a double membrane to target and engulf cell products for the formation of autophagosomes. These double membrane organelles then fuse to lysosomes where cell products are degraded and recycled (Nakamura and Yoshimori, 2018). Reports show that autophagy plays an important role in pathogen defense, development, starvation adaptations, and aging (Mizushima et al., 2008). Identifying molecular mechanisms responsible for autophagy in mammalian cells has been possible as a result of studying model systems, such as Saccharomyces cerevisiae. Autophagy related genes (Atg) are evolutionarily conserved; therefore, research of autophagy in simpler organisms have informed the roles of Atg in mammalian cells (Ruck et al., 2011; Mercer et al., 2018; Tyler and Johnson, 2018). Analysis of autophagy mutants in C. elegans revealed that
bec-1/Atg6/ Beclin 1 is essential for dauer development, a quiescent state that survives harsh conditions such as lack of nutrients, high nematode density, and high temperatures by inducing autophagy (Melndez et al., 2003; Melndez and Levine 2009).
To further investigate the phenotypes associated with the
bec-1 (
ok691) mutation, we studied nematodes possessing a 3000 base pair deletion mutation (allele
ok691) in the
bec-1 locus (Figure 1A). Previous reports show that the
bec-1 (
ok691) mutation is lethal, however a small proportion of homozygous
bec-1 (
ok691) animals reach adulthood due to maternal effect, but do not reproduce due to sterility (Figure 1B, Melendez and Levine 2009). Our analysis of survival throughout adulthood shows that lifespan is significantly reduced in homozygous
bec-1 (
ok691) mutants (Figure 1C). These nematodes do not live longer than 8 days of adulthood and 50% of animals died at day 5 of adulthood. In contrast, heterozygous
bec-1 (
ok691) mutant lifespan is not significantly different from control animals, ruling out previously discovered haploid insufficiency effects of Beclin 1 in the lifespan of C. elegans (Sinha and Levine, 2008).