Biology subjects

Lanier, A.

Publications and source records attributed to Lanier, A..

3 recordsLinked to original sources

bioRxiv2026

Comparative nectar metabolomics reveals sucrose-nitrogen tradeoffs and chemical drivers of microbial growth in floral nectar

IntroductionMany plant species secrete nectar to attract beneficial animals. The chemical composition of floral nectar influences pollinator nutrition and behavior, as well as microbial growth in flowers. Yet factors that predict nectar composition across plant species, as well as chemical compounds determining microbial growth in nectar, remain poorly understood. MethodsWe used both targeted and untargeted metabolomics to compare the nectar chemical profiles across 31 phylogenetically diverse plant species that span a range of floral morphologies. We examined the common classes of compounds detected in nectar and patterns of co-occurrence among them. We combined newly collected chemical data with previously published data on microbial growth in nectar of the same plant species to examine how nectar chemistry is associated with microbial growth. ResultsPlant species and clades varied in amino acid, minor sugar, and secondary metabolite composition and concentration. Sampled rosids and lilioids generally contained higher amino acids while asterids contained greater concentrations of oligosaccharides and sugar alcohols. Across plant species, proteinogenic amino acids frequently co-occurred in nectar but many were negatively associated with sucrose concentration. Plant species with greater concentrations of amino acids and other nitrogen-containing compounds hosted greater microbial density in nectar, while some other compound groups were negatively associated with microbial diversity. ConclusionsNegative correlations between nectar amino acid and sucrose concentration across species suggest ecological tradeoffs or physiological constraints in nectar composition. Given that the growth of common nectar microbes is limited by amino acid concentration, these findings suggest an ecological cost to amino acid production in nectar. Finally, we document variation among species in nectar vitamins, non proteinogenic amino acids and secondary metabolites with hypothesized yet currently untested ecological roles.

plant biology↗

bioRxiv2025

Anti-Parkinsonian Drugs Rescue Locomotor Deficits in JIP3 Knockout Zebrafish: Implications for Treating Patients with MAPK8IP3-related Neurodevelopmental Disorders

MAPK8IP3-related neurodevelopmental disorders are a spectrum of rare conditions caused by de novo mutations in the MAPK8IP3 gene that encodes the JIP3 protein. These disorders are associated with a spectrum of neurodevelopmental symptoms that manifest in children and cause brain abnormalities, profound intellectual disabilities, movement disorders, and developmental delays. JIP3 is required for axonal transport of proteins and organelles between the soma and the synaptic terminal of neurons, a process critical for normal brain development and function. Homozygous loss-of-function mutations in JIP3 lead to impaired axonal transport and aggregation of cargo, which result in axonal swelling and stunted elongation. Despite these severe outcomes, disease mechanisms are poorly understood, and no current treatments are available. Here we conduct thorough morphological, behavioral, and motility phenotyping in the JIP3 knockout zebrafish and identify locomotor deficits and morphological abnormalities. To identify treatment options, we used insights from expert clinicians and the artificial intelligence tool, mediKanren, to identify drug candidates hypothesized to improve patient symptoms or compensate for the loss of JIP3 at the molecular level. We then prioritized drugs that are FDA-approved, safe for children, and readily available. These collective efforts identified amantadine and levodopa as candidate therapies and rescued motor phenotypes associated with JIP3 loss-of-function in zebrafish.

neuroscience↗

bioRxiv2023

Loss of Slc35a2 alters development of the mouse cerebral cortex

Brain somatic variants in SLC35A2 are associated with clinically drug-resistant epilepsy and developmental brain malformations, including mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE). SLC35A2 encodes a uridine diphosphate galactose translocator that is essential for protein glycosylation; however, the neurodevelopmental mechanisms by which SLC35A2 disruption leads to clinical and histopathological features remain unspecified. We hypothesized that focal knockout (KO) or knockdown (KD) of Slc35a2 in the developing mouse cortex would disrupt cerebral cortical development through altered neuronal migration and cause changes in network excitability. We used in utero electroporation (IUE) to introduce CRISPR/Cas9 and targeted guide RNAs or short-hairpin RNAs to achieve Slc35a2 KO or KD, respectively, during early corticogenesis. Following Slc35a2 KO or KD, we observed disrupted radial migration of transfected neurons evidenced by heterotopic cells located in lower cortical layers and in the sub-cortical white matter. Slc35a2 KO in neurons did not induce changes in oligodendrocyte number, suggesting that the oligodendroglial hyperplasia observed in MOGHE originates from distinct cell autonomous effects. Spontaneous seizures were not observed, but intracranial EEG recordings after focal KO showed a reduced seizure threshold following pentylenetetrazol injection. These results demonstrate that Slc35a2 KO or KD in vivo disrupts corticogenesis through altered neuronal migration.

neuroscience↗