Biology subjects

Seike, K.

Publications and source records attributed to Seike, K..

4 recordsLinked to original sources

bioRxiv2025

Nectar Sugar Enhancement in Response to Bee Buzzing in Rhododendron x pulchrum: Sound-sensing Organs and Sensitivity Range

Plants can perceive and respond to airborne sounds, but our current understandings of this phenomenon remain limited. Flowers are known to exhibit increased nectar sugar concentration in response to pollinator sounds; however, there has been only a single report from Oenothera drummondii. To test the generality of pollinator-sound-induced nectar enrichment in bee-pollinated plants, we examined nectar responses to airborne sounds, particularly those produced by bee buzzing, in Rhododendron x pulchrum and Lamium amplexicaule. We exposed the flowers to playback sounds of bee buzzing, a similar synthetic sounds signal (200 Hz) and those with higher frequency (5000 Hz) and compared nectar sugar concentrations among these sound-treated and silent control flowers. We found an approximately 10% increase in nectar sugar concentration in response to playback sounds of bee buzzing and synthetic sounds signals at bee-like frequency (200 Hz), while no such response was observed under higher-frequency stimuli or silent condition in R. x pulchrum. A similar response to bee sounds was also observed in L. amplexicaule. Furthermore, these responses were observed at a sound pressure level of 65 or 100 dB, but not at 50 dB in R. x pulchrum, indicating a sound sensitivity threshold. We experimentally removed petals, stamens, or pistils (alone or in combination) from flowers and exposed them to 200 Hz sounds and silent treatments and found that both petals and stamens were necessary for such sound responses, suggesting that these floral organs are involved in acoustic sensing. Our findings provide new insights into floral sound sensing and suggest that acoustic responses to pollinator visitations may be more widespread among bee-pollinated flowering plants.

plant biology↗

bioRxiv2024

Parasitoid wasp venoms degrade Drosophila imaginal discs for successful parasitism

Parasitoid wasps, one of the most diverse and species-rich animal taxa on Earth, produce venoms that manipulate host development and physiology to exploit host resources. However, mechanisms of venom action remain poorly understood. Here, we show that infection of host Drosophila by the endoparasitoid wasp, Asobara japonica, triggers imaginal disc degradation (IDD) by inducing apoptosis, autophagy, and mitotic arrest, leading to impaired host metamorphosis. A multi-omics approach identified two venom proteins of A. japonica necessary for IDD. Knockdown experiments targeting the venom genes revealed that in concert with host immune suppression, IDD is essential for successful parasitism. Our study highlights a venom-mediated hijacking strategy of the parasitoid wasp that allows host larvae to grow, but ultimately kills the hosts.

developmental biology↗

bioRxiv2021

A redox cycle with complex II promotes sulfide quinone oxidoreductase dependent H2S oxidation

The dueling roles of H2S as an endogenously synthesized respiratory substrate and as a toxin, raise questions as to how it is cleared when the electron transport chain is inhibited. Sulfide quinone oxidoreductase (SQOR) is a mitochondrial inner membrane flavoprotein that catalyzes the first step in the H2S oxidation pathway and uses coenzyme Q (CoQ) as an electron acceptor. However, complex IV poisoning by H2S inhibits complex III-dependent recycling of CoQH2, which is needed to sustain H2S oxidation. We have discovered that under these conditions, reversal of complex II activity using fumarate as an electron acceptor, establishes a new redox cycle with SQOR. The purine nucleotide cycle and the malate aspartate shuttle are sources of fumarate in H2S treated cells, which accumulate succinate. Complex II knockdown decreases the efficiency of H2S clearance and increases recovery time to the basal respiration rate in H2S treated cells. In contrast, attenuation of complex I, which is a major competitor for the mitochondrial CoQ pool, has the opposite effects. Targeted knockout of complex II in murine intestinal epithelial cells that are routinely exposed to microbiota derived H2S, decreases serum, urine, and fecal thiosulfate, a product of H2S oxidation. Our study identifies a metabolic reprogramming response to H2S that furnishes fumarate as an alternate electron acceptor and supports H2S oxidation independent of complex IV activity. Complex II-linked redox cycling of SQOR has important implications for gut H2S metabolism as colonocytes are routinely exposed to high concentrations of this gas derived from the microbiota. One Sentence SummaryReversal of complex II sustains and prioritizes H2S oxidation when respiration is poisoned.

biochemistry↗

bioRxiv2021

Cohesin Releasing Factor WAPL Regulates Genome Structure and Function of Mature T Cells

The cohesin complex modulates gene expression and cellular functions by shaping three-dimensional (3D) organization of chromatin. WAPL, cohesins DNA release factor, regulates 3D chromatin architecture. The 3D genome structure and its relevance to mature T cell functions in vivo is not well understood. We show that in vivo lymphopenic expansion, and allo-antigen driven proliferation, alters the 3D structure and function of the genome in mature T cells. Conditional deletion of Wapl in T cells reduced long-range genomic interactions, altered chromatin A/B compartments and interactions within topologically associating domains (TADs) of the chromatin in T cells at baseline. Comparison of chromatin structure in normal and WAPL-deficient T cells after lymphopenic and allo-antigen driven stimulation revealed reduced loop extensions with changes in cell cycling genes. WAPL-mediated changes in 3D architecture of chromatin regulated activation, cycling and proliferation of T cells in vitro and in vivo. Finally, WAPL-deficient T cells demonstrated reduced severity of graft-versus-host disease (GVHD) following experimental allogeneic hematopoietic stem cell transplantation. These data collectively characterize 3D genomic architecture of T cells in vivo and demonstrate biological and clinical implications for its disruption by cohesin release factor WAPL.

molecular biology↗