RESUMEN
Metopaulias depressus is a non-marine crab endemic to Jamaica that dwells in rainforest bromeliads and exhibits elaborate active parental care behavior. Current genomic resources on M. depressus are rare, limiting the understanding of its adaptation to terrestrial life in species that evolved from marine ancestors. This study reports the complete mitochondrial genome of M. depressus assembled using Sanger sequencing. The AT-rich mitochondrial genome of M. depressus is 15,765 bp in length and comprises 13 protein-coding genes (PCGs), 2 ribosomal RNA genes, and 22 transfer RNA genes. A single 691 bp-long intergenic space is assumed to be the control region (CR) or D-loop. A set of selective pressure analyses indicate that the entirety of the PCGs experience purifying selection. Cox1, cox2, nad5, cox3, and atp6 experience strong purifying selection, and atp8 experiences weak purifying selection compared to the rest of the PCGs. The secondary structures of most tRNA genes exhibit a standard 'cloverleaf' structure, with the exception of trnS1, which lacks the dihydroxyuridine (DHU) arm but not the loop, the trnH gene, which lacks the thymine pseudouracil cytosine (T) loop but not the arm, and trnM, which exhibits an overly developed T loop. A maximum likelihood phylogenetic analysis based on all PCGs indicated that M. depressus is more closely related to the genera Clistocoeloma, Nanosesarma, and Parasesarma than to Chiromantes, Geosesarma, and Orisarma. This study contributes to deciphering the phylogenetic relationships within the family Sesarmidae and represents a new genomic resource for this iconic crab species.
Asunto(s)
Braquiuros , Genoma Mitocondrial , Animales , Braquiuros/genética , Genoma Mitocondrial/genética , Genómica , Filogenia , ARN de Transferencia/genéticaRESUMEN
St. Louis encephalitis virus (SLEV) is the prototypic mosquito-borne flavivirus in the Americas. Birds are its primary vertebrate hosts, but amplification in certain mammals has also been suggested. The place and time of SLEV emergence remain unknown. In an ecological investigation in a tropical rainforest in Palenque National Park, Mexico, we discovered an ancestral variant of SLEV in Culex nigripalpus mosquitoes. Those SLEV-Palenque strains form a highly distinct phylogenetic clade within the SLEV species. Cell culture studies of SLEV-Palenque versus epidemic SLEV (MSI-7) revealed no growth differences in insect cells but a clear inability of SLEV-Palenque to replicate in cells from birds, cotton rats, and free-tailed bats permissive for MSI-7 replication. Only cells from nonhuman primates and neotropical fruit bats were moderately permissive. Phylogeographic reconstruction identified the common ancestor of all epidemic SLEV strains to have existed in an area between southern Mexico and Panama ca. 330 years ago. Expansion of the epidemic lineage occurred in two waves, the first representing emergence near the area of origin and the second involving almost parallel appearances of the virus in the lower Mississippi and Amazon delta regions. Early diversification events overlapped human habitat invasion during the post-Columbian era. Several documented SLEV outbreaks, such as the 1964 Houston epidemic or the 1990 Tampa epidemic, were predated by the arrival of novel strains between 1 and 4 years before the outbreaks. Collectively, our data provide insight into the putative origins of SLEV, suggesting that virus emergence was driven by human invasion of primary rainforests. IMPORTANCE St. Louis encephalitis virus (SLEV) is the prototypic mosquito-transmitted flavivirus of the Americas. Unlike the West Nile virus, which we know was recently introduced into North America from the Old World, the provenience of SLEV is obscure. In an ecological investigation in a primary rainforest area of Palenque National Park, Mexico, we have discovered an ancestral variant of SLEV. The ancestral virus was much less active than the epidemic virus in cell cultures, reflecting its incomplete adaptation to hosts encountered outside primary rainforests. Knowledge of this virus enabled a spatiotemporal reconstruction of the common ancestor of all SLEVs and how the virus spread from there. We can infer that the cosmopolitan SLEV lineage emerged from Central America in the 17th century, a period of post-Columbian colonial history marked by intense human invasion of primary rainforests. Further spread followed major bird migration pathways over North and South America.