Before revision:  We show that both eukaryotic clpB amyloid disaggregases , HSP104 and its nuclear-encoded mitochondrial endo-ortholog HSP78, were lost in the stem-metazoan lineage along with only a small number of other relevant genes. We show that these gene losses are not unrelated historical accidents because these loci comprise a very small regulon devoted to prion transmission in yeast. We propose that evolution of developmental asymmetric cell-specifications necessitated the evolutionary deprecation of the ancient clpB system .
After revision:  We show that both eukaryotic clpB amyloid disaggregases , HSP104 and its nuclear-encoded mitochondrial endo-ortholog HSP78, which encode amyloid disaggregases. Despite their ancient origins in the eukaryotic and mitochondrial primogenitors, we find that both clpB loci of Saccharomyces share a promoter signature that is specific to 7 genes involved in prion homeostasis. We suggest that the loss of these amyloid disaggregases was a necessary step in the evolutionary origin of the asymmetric cell specifications of somatic development .