In yeast, phenotypic adaptations can evolve by natural selection of conformational variant prions and their variant amyloid fibers. This system requires the Hsp104 disaggregase, which fragments amyloid fibers into smaller seed prions that are passed on to mitotic descendants and meiotic spores. Interestingly, Hsp104 is found in diverse eukaryotes except metazoans. To investigate whether a prion-based transmission "genetics" was incompatible with the evolution of Metazoa , we identify genes conserved in fungi and choanoflagellates but lost in animals. 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 .
The evolution of animals involved a transition from a unicellular transcriptional regime to one supporting developmentally programmed somatic multicellularity. This transition was facilitated by an emergent developmental gene repertoire via gene family expansion and new gene innovation. Unknown, however, is whether this genomic-rewiring was constrained by genetic functions incompatible with key features of animals. Here , we identify conserved eukaryotic genes that were lost in stem-metazoans. Among the few genes lost are both eukaryotic clpB orthologs , HSP104 and 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 .
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In yeast, phenotypic adaptations can evolve by natural selection of conformational variant prions and their variant amyloid fibers. This system requires the Hsp104 disaggregase, which fragments amyloid fibers into smaller seed prions that are passed on to mitotic descendants and meiotic spores. Interestingly, Hsp104 is found in diverse eukaryotes except metazoans. To investigate whether a prion-based transmission "genetics" was incompatible with the evolution of Metazoa
The evolution of animals involved a transition from a unicellular transcriptional regime to one supporting developmentally programmed somatic multicellularity. This transition was facilitated by an emergent developmental gene repertoire via gene family expansion and new gene innovation. Unknown, however, is whether this genomic-rewiring was constrained by genetic functions incompatible with key features of animals. Here
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genes conserved in fungi and choanoflagellates but lost in animals. We show that
conserved eukaryotic genes that were lost in stem-metazoans. Among the few genes lost are
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amyloid disaggregases
orthologs
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its nuclear-encoded mitochondrial endo-ortholog
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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
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