Biology subjects

Velasquez, M.

Publications and source records attributed to Velasquez, M..

3 recordsLinked to original sources

bioRxiv2026

Operationalizing site-level conservation for migratory birds across the Americas flyways

Conserving migratory birds effectively requires full annual cycle strategies that identify where on-the-ground efforts can have the greatest impact. Here, we present a hemispheric spatial framework to identify priority areas for 112 migratory bird species across the Americas. Building on full annual cycle prioritizations, we defined finer-scale spatial planning units that reflect differences in migratory and congregational behaviors between shorebirds and landbirds. We compiled population data for each planning unit and focal species and applied conservation planning tools to design area-efficient portfolios of sites and landscapes that secure 10% of each species population within the Americas flyways. The resulting minimum area portfolios include 175 shorebird sites and 80 landbird landscapes optimized to meet the species-specific 10% representation targets across breeding, non-breeding, and passage seasons. We also identified a broader set of complementary solutions, ranked by an importance score, to provide decision-makers with flexible options for strategic resource allocation. This framework provides the scientific foundation for the Americas Flyways Initiative (AFI), which aims to catalyze investment in nature-based solutions and bird-friendly infrastructure to enhance the conservation of migratory birds and strengthen the resilience of the Americas flyways by 2050.

ecology↗

bioRxiv2026

Hormonal control of postmitotic neuronal identity

Developmental transcriptional programs establish neuronal diversity and circuit assembly, but how these regulators continue to shape and preserve neuronal identity remains unresolved. The Drosophila central complex comprises precisely wired circuits of diverse neuronal types that coordinate complex behaviors. Within this structure, dorsal fan-shaped body (dFB) neurons integrate internal-state signals to regulate sleep, feeding, and energy homeostasis, yet how distinct dFB subtypes are specified and maintained remains unknown. More broadly, whether developmental transcription factors continue to act in mature neurons to preserve neuronal identity is poorly understood. Here, we define the developmental origin and molecular regulation of neuronal identity in 84C10-labelled dFB neurons that innervate layers 6-7 of the FB and contribute to nutrient sensing and metabolic adaptation. Using lineage tracing, clonal analysis, and birth dating, we show that dFB neurons are generated late in development and arise from two distinct type II neural stem cell lineages, dorsolateral 1 and dorsomedial 4. These dFB neurons continue to express the late temporal transcription factor, ecdysone-induced protein 93 (E93), in adulthood. Post-mitotic depletion of E93 results in progressive neuronal loss and ectopic expansion of axonal arborizations across FB layers and, notably, a marked reduction in vesicular glutamate transporter (vGLUT) expression. These defects are accompanied by impaired increases in fat-to-lean mass ratios in response to high-sugar feeding. Together, our findings identify E93 as a post-mitotically retained temporal transcription factor that maintains neuronal survival, laminar connectivity, and neurotransmitter identity, revealing that developmental temporal programs are redeployed in adulthood to sustain neuronal identity and function.

neuroscience↗

bioRxiv2022

Quantitative imaging of gene therapy delivery vehicles using CEST-NMR/MRI

PurposeGene therapy employing AAV vector-mediated gene delivery has undergone substantial growth in recent years with promising results in both preclinical and clinical studies, as well as emerging regulatory approval. However, the lack of methods for quantifying the efficacy of gene therapy from cellular delivery of gene editing technology to specific functional outcomes remains an obstacle for the efficient development of gene therapy treatments. Building upon prior works that utilized a genetically encoded Lysine Rich Protein as a chemical exchange saturation transfer (CEST) reporter, we hypothesized that AAV viral capsids may generate endogenous CEST contrast from the large number of surface lysine residues. MethodsWater-suppressed NMR and NMR-CEST experiments were performed on isolated solutions of AAV serotypes 1-9 on a Bruker 800MHz vertical scanner. A series of in vitro experiments were performed for thorough testing of NMR-CEST contrast of AAV2 capsids under varying pH, density, biological transduction stage, and later across multiple serotypes and mixed biological media. Reverse transcriptase (RT)-polymerase chain reaction (PCR) was used to quantify virus concentration. Subsequent experiments determined the pH-dependent exchange rate and optimized CEST saturation schemes for AAV contrast detection at 7 T. ResultsNMR-CEST experiments revealed CEST contrast up to 52% for AAV2 viral capsids between 0.6-0.8 ppm. Evaluation of CEST contrast generated by AAV2 demonstrates high levels of CEST contrast across a variety of chemical environments, concentrations, and saturation schemes. AAV2 CEST contrast displayed significant positive correlations with capsid density (R2>0.99, P<0.001), pH (R2=0.97, P=0.01), and viral titer per cell count (R2=0.92, P<0.001). Transition to a preclinical field strength yielded up to 11.8% CEST contrast following optimization of saturation parameters. ConclusionAAV2 viral capsids exhibit strong capacity as an endogenous CEST contrast agent and can potentially be used for monitoring and evaluation of AAV vector-mediated gene therapy protocols.

bioengineering↗