Valentina Botero

ORCID: 0000-0002-9744-3929
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About
Contact & Profiles
Research Areas
  • Neurobiology and Insect Physiology Research
  • Neurofibromatosis and Schwannoma Cases
  • Hippo pathway signaling and YAP/TAZ
  • Insect Utilization and Effects
  • Circadian rhythm and melatonin
  • Sleep and Wakefulness Research
  • Insect and Arachnid Ecology and Behavior
  • Vascular Malformations Diagnosis and Treatment
  • RNA and protein synthesis mechanisms
  • Water resources management and optimization
  • RNA regulation and disease
  • Neuroblastoma Research and Treatments
  • Retinal Development and Disorders
  • Ferroelectric and Negative Capacitance Devices
  • Genetics and Neurodevelopmental Disorders
  • Water-Energy-Food Nexus Studies
  • Signaling Pathways in Disease
  • Cellular transport and secretion

University of Iowa
2022-2025

Scripps Research Institute
2019-2022

Scripps Institution of Oceanography
2022

Anatomical and physiological compartmentalization of neurons is a mechanism to increase the computational capacity circuit, major question what role axonal plays. Axonal may enable localized, presynaptic plasticity alter neuronal output in flexible, experience-dependent manner. Here, we show that olfactory learning generates compartmentalized, bidirectional acetylcholine release varies across longitudinal compartments Drosophila mushroom body (MB) axons. The directionality learning-induced...

10.7554/elife.76712 article EN cc-by eLife 2022-03-14

Genetic disorders such as neurofibromatosis type 1 increase vulnerability to cognitive and behavioral disorders, autism spectrum disorder attention-deficit/hyperactivity disorder. Neurofibromatosis results from mutations in the neurofibromin gene that can reduce levels of protein (Nf1). While mechanisms have yet be fully elucidated, loss Nf1 may alter neuronal circuit activity leading changes behavior susceptibility comorbidities. Here we show decreasing expression motor behaviors, impacting...

10.1523/jneurosci.1531-24.2025 article EN Journal of Neuroscience 2025-02-18

How changes in brain scaling relate to altered behavior is an important question neurodevelopmental disorder research. Mice with germline Pten haploinsufficiency (Pten+/-) closely mirror the abnormal and behavioral deficits seen humans macrocephaly/autism syndrome, which caused by PTEN mutations. We explored whether deviation from normal patterns of growth can predict abnormalities. Brain regions associated sensory processing (e.g., pons inferior colliculus) had biggest deviations expected...

10.1016/j.isci.2022.103796 article EN cc-by iScience 2022-01-19

Abstract Neurofibromatosis type 1 is a chronic multisystemic genetic disorder that results from loss of function in the neurofibromin protein. Neurofibromin may regulate metabolism, though underlying mechanisms remain largely unknown. Here we show regulates metabolic homeostasis Drosophila via discrete neuronal circuit. Loss increases rate Ras GAP-related domain-dependent mechanism, feeding homeostatically, and alters lipid stores turnover kinetics. The increase independent locomotor...

10.1038/s41467-021-24505-x article EN cc-by Nature Communications 2021-07-13

Neurofibromatosis type 1 is a monogenetic disorder that predisposes individuals to tumor formation and cognitive behavioral symptoms. The neuronal circuitry developmental events underlying these neurological symptoms are unknown. To better understand how mutations of the gene (NF1) drive alterations, we have examined grooming in Drosophila neurofibromatosis model. Mutations fly NF1 ortholog excessive grooming, increased was observed adults when Nf1 knocked down during development....

10.1371/journal.pgen.1008920 article EN cc-by PLoS Genetics 2020-07-22

Neural regulation of sleep and metabolic homeostasis are critical in many aspects human health. Despite extensive epidemiological evidence linking dysregulation with obesity, diabetes, syndrome, little is known about the neural molecular basis for integration function. The RAS GTPase-activating gene Neurofibromin ( Nf1 ) has been implicated rate, raising possibility that it serves to integrate these processes, but effects on consolidation physiology remain poorly understood. A key hallmark...

10.1371/journal.pgen.1011049 article EN cc-by PLoS Genetics 2023-12-13

Abstract Genetic disorders such as neurofibromatosis type 1 increase vulnerability to cognitive and behavioral disorders, autism spectrum disorder attention-deficit/hyperactivity disorder. Neurofibromatosis results from loss-of-function mutations in the neurofibromin gene subsequent reduction protein (Nf1). While mechanisms have yet be fully elucidated, loss of Nf1 may alter neuronal circuit activity leading changes behavior susceptibility comorbidities. Here we show that decreasing...

10.1101/2024.08.08.607070 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-08-09

Abstract Neural regulation of sleep and metabolic homeostasis are critical in many aspects human health. Despite extensive epidemiological evidence linking dysregulation with obesity, diabetes, syndrome, little is known about the neural molecular basis for integration function. The RAS GTPase-activating gene Neurofibromin ( Nf1 ) has been implicated rate, raising possibility that it serves to integrate these processes, but effects on consolidation physiology remain poorly understood. A key...

10.1101/2022.09.15.508161 preprint EN cc-by-nc bioRxiv (Cold Spring Harbor Laboratory) 2022-09-19

ABSTRACT Neurofibromatosis type 1 (NF1) is a genetic disorder predisposing patients to range of features, the most characteristic which include areas abnormal skin pigmentation and benign tumors associated with peripheral nerves, termed neurofibromas. Less common, but more serious symptoms also malignant nerve sheath tumors, other malignancies, learning disabilities. The NF1 gene encodes neurofibromin, large protein that functions as negative regulator Ras signaling mediates pleiotropic...

10.1101/834788 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-11-08
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