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Batista, J.

Publications and source records attributed to Batista, J..

5 recordsLinked to original sources

Historical biogeography and population genetic structure of the giant gilded catfish (Brachyplatystoma rousseauxii): expanding Humboldtian connectivity routes between the Orinoco and Amazon River basins

Understanding the evolutionary history of species within a geographic context is key to historical biogeography, as it reveals how geological and climatic changes shaped biodiversity. This is especially important in ecologically significant regions like the Amazon and Orinoco basins. Together, they host the worlds greatest freshwater fish diversity ([~]3,500 species), sharing a common but not yet fully understood evolutionary history. The gilded catfish (Brachyplatystoma rousseauxii), an ancient species widely distributed as a metapopulation in Neotropics, is an important model for studying past connectivity, divergence, and historical processes shaping fish diversity between these basins. This study analyzed the genetic structure, connectivity routes, and demographic history of B. rousseauxii using nuclear (microsatellite and ddRADseq) and mitochondrial DNA. Population structure analyses and coalescent models indicate that B. rousseauxii populations from the Orinoco and Amazon basins are genetically distinct, with no evidence of current gene flow. However, our results support the occurrence of a possible secondary contact event after the divergence, with the Boa Vista population retaining the genetic signal of this process. The ancestral population split occurred at the Rupununi Portal around 2.54 Ma (ddRAD) or 1.31 Ma (mtDNA). Then, the species colonized the Branco and Orinoco Rivers [~]1.90 Ma (ddRAD) or 0.6 Ma (mtDNA), rapidly expanding in the Orinoco (>1.3 or >0.29 Ma), while colonization of the Amazon from the Branco River was more recent ([≤]1.0 or [≤]0.15 Ma). Population expansion signal was detected in the Orinoco ([~]0.20 Ma), whereas the Amazon remained stable. Our findings suggest that the rise of the Vaupes Arch in the Late Miocene does not explain the observed genetic divergence. Likewise, the Casiquiare Canal and Japura-Guaviare headwaters are not connectivity routes between basins. Instead, the Rupununi Portal, including the recent capture of the Branco River by the Negro River, was the last point of connection and played a key role in shaping B. rousseauxiis distribution. These findings provide insights into Neotropical fish biogeography and the historical configuration of the Orinoco and Amazon basins.

evolutionary biology↗

The tumor suppressor Tip60 inhibits TORC1 signaling in response to microbial acetate to promote autophagy and enterocyte differentiation

The intestinal microbiota is critical for maintenance of local and systemic immune and metabolic homeostasis in animals, but few molecular mechanisms of action have been delineated. Here, using a Drosophila model, we elucidate the role of the microbial fermentation product acetate in maintenance of the intestinal barrier and enterocyte maturation. Tip60 is a lysine acetyl transferase that modifies histone and non-histone targets. We previously showed that Tip60 activates innate immune signaling in enteroendocrine cells in response to microbe-derived acetate. Here we elucidate a distinct mechanism of action in enterocytes. mTOR is a serine-threonine kinase that regulates cell growth and autophagy based on nutrient availability as part of the TORC1 complex. We report that microbe-derived acetate represses enterocyte TORC1 signaling in a Tip60-dependent manner. This licenses autophagy, which is required to destroy commensal microbes phagocytosed by enterocytes, resulting in bacterial dissemination. Single cell sequencing shows accumulation of poorly differentiated enterocytes in Tip60 knockdown intestines. The microbiota, Tip60, and mTOR have been implicated in the development and progression of colorectal cancer. As accumulation of undifferentiated precursors is a harbinger of malignant transformation and metastasis, we propose our findings provide a mechanistic link between the microbiota, Tip60, and mTOR, epithelial innate immunity and oncogenesis.

immunology↗

Extreme phenotypes define epigenetic and metabolic signatures in cardiometabolic syndrome.

Improving the understanding of cardiometabolic syndrome pathophysiology and its relationship with thrombosis are ongoing healthcare challenges. Using plasma biomarkers analysis coupled with the transcriptional and epigenetic characterisation of cell types involved in thrombosis, obtained from two extreme phenotype groups (obese and lipodystrophy) and comparing these to lean individuals and blood donors, the present study identifies the molecular mechanisms at play, highlighting patterns of abnormal activation in innate immune phagocytic cells and shows that extreme phenotype groups could be distinguished from lean individuals, and from each other, across all data layers. The characterisation of the same obese group, six months after bariatric surgery shows the loss of the patterns of abnormal activation of innate immune cells previously observed. However, rather than reverting to the gene expression landscape of lean individuals, this occurs via the establishment of novel gene expression landscapes. Netosis and its control mechanisms emerge amongst the pathways that show an improvement after surgical intervention. Taken together, by integrating across data layers, the observed molecular and metabolic differences form a disease signature that is able to discriminate, amongst the blood donors, those individuals with a higher likelihood of having cardiometabolic syndrome, even when not presenting with the classic features.

genomics↗

CYRI (FAM49) proteins are local inhibitors of Scar/WAVE induced lamellipodia that bind directly to active Rac1

Actin-based protrusions driving cell migration are reinforced through positive feedback, but it is unclear how the cell restricts the eventual size of a protrusion or limits positive signals to cause splitting or retraction. We have identified an evolutionarily conserved regulator of the protrusion machinery, which we name CYRI (CYFIP-related Rac interacting) protein. CYRI shows sequence similarity to the Scar/WAVE complex member CYFIP in a Domain of Unknown Function, DUF1394. CYRI binds specifically to activated Rac1 via a common motif shared with CYFIP, establishing DUF1394 as a new Rac1 binding domain. CYRI-depleted cells have broad, Scar/WAVE-enriched lamellipodia and enhanced Rac1 signaling. Conversely, CYRI overexpression suppresses spreading and dramatically sharpens protrusions into unproductive needles. CYRI proteins use dynamic inhibition of Scar/WAVE induced actin to focus positive protrusion signals and regulate pseudopod complexity. CYRI behaves like a \"local inhibitor\" predicted and described in widely accepted mathematical models, but not previously identified in living cells.

cell biology↗

Rampant Reverse Evolution towards Specialization in Commensal Bacteria Colonizing the Gut

The maintenance of diversity in the gut microbiota is a signature of host health. Yet how strain variation emerges and changes over time in this ecosystem is poorly understood. Here we use a natural yet controlled system to track the effects of natural selection by the genetic signatures it leaves in evolving populations. By following the emergence of intra-species diversity in an Escherichia coli strain, we unravel a recurrent case of violation of Dollos law, which proposes that evolution is unidirectional and irreversible. We demonstrate de novo acquisition of a primordial lost phenotype via compensatory mutation and also genetic reversion, the latter leaving no trace of the past. We show that this reverse evolution generates two coexisting phenotypes, resource generalist and specialist, whose abundance can be controlled by diet supplementation. While specialists abundance is low, they avoid competition with the gut microbiota, whereas generalist abundance is dependent on microbiota composition. Our results highlight how a single genetic change can have large ecological consequences.

evolutionary biology↗