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Yasunaga, A.

Publications and source records attributed to Yasunaga, A..

2 recordsLinked to original sources

Divergent mechanics of inner ear morphogenesis are coupled to developmental tempo over vertebrate evolution

Vertebrate embryos vary in size and developmental tempo based on reproductive strategies; however, organs of ancient origin, such as the eye and inner ear, remain highly conserved in structure and function. How both diverse embryonic traits and conserved organ development occur remains unclear. Here, we identify divergent morphogenetic mechanics of inner ear development, particularly in vesicular primordium expansion, in 12 species representing the major vertebrate lineages. Differences in cell volume regulation determine tissue growth mechanics, which diversify the expansion process but yield a conserved morphological outcome. Heterochronic shifts in organogenesis allow this regulation to evolve in coordination with a prolonged developmental period. These findings suggest that alternative morphogenetic mechanics mitigate the effects of diversified embryonic traits, thereby ensuring consistent morphological outcomes for highly conserved organs.

evolutionary biology↗

Leishmania amazonensis sabotages host cell SUMOylation for intracellular survival

Leishmania parasites use elaborate virulence mechanisms to invade and thrive in macrophages. These virulence mechanisms inhibit host cell defense responses and generate a specialized replicative niche, the parasitophorous vacuole. In this work, we performed a genome-wide RNAi screen in Drosophila macrophage-like cells to identify host factors necessary for Leishmania amazonensis infection. This screen identified 52 conserved genes required specifically for parasite entry, including several components of the SUMOylation machinery. Further studies in mammalian macrophages found that L. amazonensis infection inhibited SUMOylation within infected macrophages and this inhibition enhanced parasitophorous vacuole growth and parasite proliferation through modulation of multiple genes especially ATP6V0D2, which in turn effects CD36 expression and cholesterol levels. Together, these data suggest that parasites actively sabotage host SUMOylation and alter host transcription to improve their intracellular niche and enhance their replication.

cell biology↗