The ability to evolve is a key characteristic that distinguishes living things from non-living chemical compounds. The construction of an evolvable cell-like system entirely from non-living molecules has been a major challenge. Here we construct an evolvable artificial cell model from an assembly of biochemical molecules. The artificial cell model contains artificial genomic RNA that replicates through the translation of its encoded RNA replicase. We perform a long-term (600-generation) replication experiment using this system, in which mutations are spontaneously introduced into the RNA by replication error, and highly replicable mutants dominate the population according to Darwinian principles. During evolution, the genomic RNA gradually reinforces its interaction with the translated replicase, thereby acquiring competitiveness against selfish (parasitic) RNAs. This study provides the first experimental evidence that replicating systems can be developed through Darwinian evolution in a cell-like compartment, even in the presence of parasitic replicators.

Background: Deficiencies in ␤-D-galactosidase cause lysosomal storage diseases. Results: This is the first report to describe the crystal structure of human ␤-Gal. Human ␤-Gal is composed of a TIM barrel domain and two ␤-domains. Conclusion: The mutations were classified as mutations directly affecting the ligand recognition, mutations inside the protein core, or mutations located in the protein surface. Significance: Structural insights into lysosomal storage diseases mutations can be demonstrated.

Background:The pathogenic mechanism of Serratia marcescens is poorly understood. Results: S. marcescens kills immune cells via an lipopolysaccharide-and flagella-dependent mechanism. Conclusion: S. marcescens suppresses innate immunity by killing immune cells.Significance: This is the first evidence to suggest that S. marcescens evades the immune system.

Single-stranded RNA (ssRNA) is the simplest form of genetic molecule and constitutes the genome in some viruses and presumably in primitive life-forms. However, an innate and unsolved problem regarding the ssRNA genome is formation of inactive double-stranded RNA (dsRNA) during replication. Here, we addressed this problem by focusing on the secondary structure. We systematically designed RNAs with various structures and observed dsRNA formation during replication using an RNA replicase (Qβ replicase). From the results, we extracted a simple rule regarding ssRNA genome replication with less dsRNA formation (less GC number in loops) and then designed an artificial RNA that encodes a domain of the β-galactosidase gene based on this rule. We also obtained evidence that this rule governs the natural genomes of all bacterial and most fungal viruses presently known. This study revealed one of the structural design principles of an ssRNA genome that replicates continuously with less dsRNA formation.