Autophagy comprises one of the intracellular degradation systems conserved from yeasts to humans. This system plays a vital role in the degradation of intracellular components such as proteins and organelles in the processes of their exclusion and turnover. Autophagy is also necessary for adaptation to environmental changes, including depletion of various nutrients. Till date, several autophagy-related genes and mechanisms have been identified, wherein the budding yeast Saccharomyces cerevisiae has significantly contributed to this identification (Mizushima et al., 2011; Ohsumi, 2014; Xie & Klionsky, 2007). Although autophagy is widely conserved, there exist some differences in the conditions that induce autophagy and its related factors among species. For instance, autophagy is induced by carbon depletion in S. cerevisiae, but not in Schizosaccharomyces pombe (Mukaiyama et al., 2009). Moreover, autophagy factors are partially different between these two species (Mukaiyama et al., 2010). Yeasts have also contributed to lifespan studies, and a chronological lifespan is defined as the survival period after entry into the stationary phase (Fabrizio & Longo, 2003). Earlier, the Ecl1 family genes (ecl1 + , ecl2 + and ecl3 + , respectively) were identified whose over-expression was found to cause the extension of the chronological lifespan in S. pombe (Ohtsuka et al., 2008, 2009). These genes encode small proteins consist of about 80 amino acids, respectively, but their molecular functions have been unclear. However, phenotypic analysis revealed that Ecl1 family genes are also essential for the appropriate cellular response to sulfur depletion (Ohtsuka et al., 2017). Sulfur is one of the essential nutrients and is present in sulfur compounds such as biotin, thiamine, coenzyme A, lipoic acid and sulfur amino acid. Sulfur depletion induces cellular responses such as lifespan extension, morphological changes, and cell cycle arrest in S. pombe, and these phenomena are almost completely dependent on the Ecl1 family genes (Ohtsuka et al., 2017).