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Kuroda, J.

Publications and source records attributed to Kuroda, J..

4 recordsLinked to original sources

Actinotrichia-independent developmental mechanisms of spiny rays facilitate the morphological diversification of Acanthomorpha fish fins

Skeletal forms in vertebrates have been regarded as good models of morphological diversification. Fish fin forms are greatly diversified, and their bone structure is classified into soft rays and spiny rays. In fish evolution, spiny-ray morphologies are known to be sometimes extremely modified; however, it remains unknown how the developmental mechanisms of spiny-rays have contributed to their morphological diversification. By using the rainbowfish Melanotaenia praecox for examination of the extracellular matrix (ECM) and cell dynamics of spiny-ray development, we demonstrate that spiny-ray developments are independent of the actinotrichia (needle-shaped collagen polymers at the tip of fish fins), which are known as an important ECM in soft-ray morphogenesis. Furthermore, we found that in the thorny spiny-ray of the filefish Stephanolepis cirrhifer, the lateral protrusions equip the BMP positive osteoblast condensation, as in the state of the spiny-ray tips in M. praecox and S. cirrhifer. Taken together, our findings reveal that osteoblast distribution and signaling-molecule intensity would contribute to spiny-ray modification. In comparison to soft rays development, the independence from actinotrichia in spiny-rays would facilitate growth direction change, leading to their morphological diversification. This indicates that the cell distribution and ECM usage would be major factors driving the morphological diversification in animals.

evolutionary biology↗

Pain-stimulated ultrasound vocalizations and their impact on pain response in mice

Pain is a complex phenomenon encompassing both the physiological and psychological aspects of sensation and emotion, respectively. In recent years, pain has been clarified to arise even without direct injury, with emotional transmission as a cause. However, the specific mechanisms behind emotional transmission are still not well understood. In this study, sounds in the ultrasonic domain that were recorded during pain stimulation in mice were used as sound stress to examine the effects of psychological stress caused by exposure to ultrasound on tactile thresholds. We also examined the effects of psychological stress caused by the ultrasound on an inflammatory pain model of mice. The tactile threshold decreased the next and three days after sound stress exposure in mice. DNA microarray analysis of the mouse thalamus exposed to sound stress revealed increased expression of inflammation-related genes, Prostaglandin-endoperoxide synthase 2 and C-X-C motif chemokine ligand 1. Their respective inhibitors, loxoprofen and SB225002, significantly improved hyperalgesia induced by sound stress. When sound stress was applied to a mouse model of inflammatory pain in which pain thresholds were restored 14 days after complete Freunds adjuvant administration, prolonged pain and attenuated analgesic effects of loxoprofen were observed. These results suggest that sound stress not only induces inflammation in the brain that causes hyperalgesia but may also be partially responsible for exacerbating inflammatory pain, hence complicating treatment.

pharmacology and toxicology↗

In Vivo Imaging of Bone Collagen Dynamics in zebrafish

Type I collagen plays a pivotal role in shaping bone morphology and determining its physical properties by serving as a template for ossification. Nevertheless, the mechanisms underlying bone collagen formation, particularly the principles governing its orientation, remain unknown due to the lack of a method enabling continuous in vivo observation. To address this challenge, we constructed a method to visualize bone collagen by tagging with GFP in zebrafish and observed the interactions between the osteoblasts and collagen fiber during bone formation in vivo. When Col1a2-GFP was expressed under the control of the osteoblast-specific promoters osx or osc in zebrafish, bone collagen could be observed clearly enough to identify their localization, but collagen from other organs did not. Therefore, we determined that this method was of sufficient quality for detailed in vivo observation of bone collagen. Next, bone collagen in the scales, fin ray, and opercular bones was observed in detail in zebrafish, when bone formation is more active. By simultaneously observing bone collagen and osteoblasts, we successfully observed dynamic changes in the morphology and position of osteoblasts from the early stages of bone formation. It was also found that the localization pattern and orientation of bone collagen significantly differed depending on the choice of expression promoter. Both promoters (osx and osc) used in this study are osteoblast-specific, but their Col1a2-GFP localizing regions within bone are exclusive, with osx region localizing mainly the outer edge of bone and osc region localizing the central area of bone. This suggests the existence of distinct subpopulations of osteoblasts with various gene expression profiles, each of which may play a unique role in the osteogenic process. These findings would contribute to a better understanding of the mechanisms governing bone collagen formation by osteoblasts.

cell biology↗

The Drosophila AWP1 ortholog Doctor No regulates JAK/STAT signaling for left-right asymmetry in the gut by promoting receptor endocytosis

Many internal Drosophila organs show stereotypical left-right (LR) asymmetry, for which the underlying mechanisms remain elusive. Here, we identified an evolutionarily conserved ubiquitin-binding protein, AWP1/Doctor no (Drn), as a novel factor required for the LR asymmetry of the embryonic anterior gut in Drosophila. We showed that drn is essential in the circular visceral muscle cells of the midgut for JAK/STAT signaling, which contributes to the first known cue for anterior gut lateralization via LR-asymmetric nuclear rearrangement. Embryos homozygous for drn and lacking its maternal contribution showed phenotypes similar to that of depleted JAK/STAT signaling, suggesting that Drn is a general component of JAK/STAT signaling. The absence of Drn resulted in the specific accumulation of Domeless (Dome), the receptor of JAK/STAT signaling, in intracellular compartments. Thus, Drn is required for the endocytic trafficking of Dome, which is subsequently degraded in lysosomes. Our results suggest that the endocytosis of Dome is a critical step in activating JAK/STAT signaling. The roles of AWP1/Drn in activating JAK/STAT signaling and in LR-asymmetric development may be conserved in various organisms. Summary StatementDr. No, a Drosophila ortholog of AWP1, activates JAK/STAT signaling via Dome receptor endocytosis in a crucial step for left-right asymmetry in the developing gut.

developmental biology↗