Biology subjects

Omura, K.

Publications and source records attributed to Omura, K..

4 recordsLinked to original sources

bioRxiv2026

Molecular evolutionary evidence for coexistence within oak hybrid zones.

Resource allocation trade-offs in seedlings have been widely proposed to facilitate the coexistence of tree species; however, whether selection can maintain the underlying genetic variation under gene flow remains insufficiently investigated. Using a natural hybrid zone between two East Asian oaks, we evaluated whether loci associated with allocation trade-offs showed signatures of selection despite hybridisation. Acorns collected across the zone were cultivated in a common garden, where we quantified 25 seedling growth and functional traits, and analysed whole-genome variation. We identified trade-offs between leaf function and plant architecture. Trait-associated genomic regions demonstrated strong inter-chromosomal linkage disequilibrium in the hybrids, consistent with genetic coupling, and exhibited elevated interspecific differentiation and more pronounced genetic clines. These results indicate that multilocus selection counteracts gene flow through the development of genetic coupling, thereby maintaining resource allocation trade-offs that may contribute to tree coexistence.

evolutionary biology↗

bioRxiv2026

LeafContourEFD: a reproducible workflow for elliptic Fourier analysis with orientation normalization and lateral asymmetry

PremiseElliptic Fourier analysis is widely used to quantify leaf shape variation, but inconsistent normalization and orientation alignment can introduce biologically irrelevant variation. In addition, a reproducible workflow from raw images to normalized elliptic Fourier descriptors (EFDs) is still lacking. Methods and ResultsWe developed LeafContourEFD, a GUI application for reproducible leaf morphometrics. It integrates image segmentation, contour extraction, EFD calculation, and an extended normalization framework, termed oriented true EFD normalization, based on a user-defined biological reference axis. Analyses of Quercus serrata, Q. crispula, and Triadica sebifera showed that existing normalization methods can introduce orientation-related variance when the first-harmonic major axis does not match the leaf base-to-tip axis. In contrast, oriented true normalization removed these artifacts, yielding clearer shape transitions along principal components allowing shape variation among leaves to be captured while preserving biologically meaningful lateral asymmetry. ConclusionsLeafContourEFD improves interpretability and reproducibility in outline-based morphometrics and provides transparent outputs and metadata for data sharing and cross-study comparisons.

plant biology↗

bioRxiv2025

An intercellular signaling pathway in the mouse retina connects Kv2.1, GLT-1, and nitric oxide synthase 1 to optic nerve regeneration

We report here that a multicellular signaling pathway in the mouse retina targeting glutamate homeostasis and nitric oxide production is activated upon optic nerve injury and modulates reti-nal ganglion cells (RGCs) ability to mount a robust regenerative response. A novel highly sen-sitive and specific NO sensor (FL2) revealed that optic nerve injury leads to a rapid, prolonged elevation of NO in the inner retina. Amacrine cell-specific genetic deletion of the neuron-specific isoform of nitric oxide synthase (NOS1, nNOS) or the NOS1 inhibitor N(w)-propyl-L-arginine (L-NPA) suppressed optic nerve regeneration. Steps leading to NOS1 activation are shown to in-clude Kv2.1 phosphorylation and activation, reversal of glutamate uptake by the glutamate transporter GLT-1 (EAAT2), and subsequent NMDA receptor activation. Conditional knockout of the glutamate transporter GLT-1 in bipolar cells, intraocular injection of the GLT-1 blockers dihydrokainate (DHK) or WAY213613, the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovalerate (D-AP5), or the Kv2.1 blockers RY796 or stromatoxin all sup-pressed NO generation and strongly diminished RGCs ability to respond to Pten deletion and other factors. Thus, optic nerve injury activates a sequence of pathophysiological changes in retinal interneurons that gates RGCs ability to regenerate injured axons. Significance StatementCells use extracellular signals to coordinate responses to injury and to promote repair and re-generation. The NMDA receptor, which has a high affinity for glutamate and is functionally cou-pled to nitric oxide synthase, has the potential to mediate such responses by responding to changes in extracellular glutamate. In the mouse retina after optic nerve injury, potassium channels in retinal ganglion cells, glutamate transporters in neighboring cells, and NMDA recep-tors in amacrine cells, are all involved in a pathway that regulates the generation of nitric oxide, which we show promotes axon regeneration after injury.

neuroscience↗

bioRxiv2018

Combined inhibition of apoptosis and necrosis promotes transient neuroprotection of retinal ganglion cells and partial axon regeneration after optic nerve damage

Retinal ganglion cell (RGC) death is the hallmark of glaucoma. Axonal injury is thought to precede RGC loss in glaucoma, and thus studies using an optic nerve (ON) crush model have been widely used to investigate mechanisms of cell death that are common to both conditions. Prior work has focused on the involvement of caspases in RGC death, but little is known about the contribution of other forms of cell death such as necrosis. In this study we show that receptor interacting protein (RIP) kinase-mediated necrosis normally plays a role in RGC death and acts in concert with caspase-dependent apoptosis. The expression of RIP3, a key activator of RIP1 kinase, as well as caspase activity, increased following ON injury. Caspase inhibition alone failed to provide substantial protection to injured RGCs and unexpectedly exacerbated necrosis. In contrast, pharmacologic or genetic inhibition of RIP kinases in combination with caspase blockade delayed both apoptotic and necrotic RGC death, although RGCs still continued to die. Furthermore, inhibition of RIP1 kinase promoted a moderate level of axon regeneration that was only minimal affected by caspase inhibition. In conclusion, multiple approaches are required for effective RGC death prevention and axonal regeneration. Further studies are needed to elucidate more effective long term strategies that can lead to sustained neuroprotection and regeneration.

neuroscience↗