Taro Fukazawa

Early fin primordia of zebrafish larvae regenerate by a similar growth control mechanism with adult regeneration.

Some vertebrate species, including urodele amphibians and teleost fish, have the remarkable ability of regenerating lost body parts. Regeneration studies have been focused on adult tissues, because it is unclear whether or not the repairs of injured tissues during early developmental stages have the same molecular base as that of adult regeneration. Here, we present evidence that a similar cellular and molecular mechanism to adult regeneration operates in the repair process of early zebrafish fin primordia, which are composed of epithelial and mesenchymal cells. We show that larval fin repair occurs through the formation of wound epithelium and blastema‐like proliferating cells. Cell proliferation is first induced in the distal‐most region and propagates to more proximal regions, as in adult regeneration. We also show that fibroblast growth factor signaling helps induce cell division. Our results suggest that the regeneration machinery directing cell proliferation in response to injury may exist from the early developmental stages. Developmental Dynamics 231:693–699, 2004.

Acute phase response in amputated tail stumps and neural tissue-preferential expression in tail bud embryos of the Xenopus neuronal pentraxin I gene

Regeneration of lost organs involves complex processes, including host defense from infection and rebuilding of lost tissues. We previously reported that Xenopus neuronal pentraxin I (xNP1) is expressed preferentially in regenerating Xenopus laevis tadpole tails. To evaluate xNP1 function in tail regeneration, and also in tail development, we analyzed xNP1 expression in tailbud embryos and regenerating/healing tails following tail amputation in the ‘regeneration’ period, as well as in the ‘refractory’ period, when tadpoles lose their tail regenerative ability. Within 10 h after tail amputation, xNP1 was induced at the amputation site regardless of the tail regenerative ability, suggesting that xNP1 functions in acute phase responses. xNP1 was widely expressed in regenerating tails, but not in the tail buds of tailbud embryos, suggesting its possible role in the immune response/healing after an injury. xNP1 expression was also observed in neural tissues/primordia in tailbud embryos and in the spinal cord in regenerating/healing tails in both periods, implying its possible roles in neural development or function. Moreover, during the first 48 h after amputation, xNP1 expression was sustained at the spinal cord of tails in the ‘regeneration’ period tadpoles, but not in the ‘refractory’ period tadpoles, suggesting that xNP1 expression at the spinal cord correlates with regeneration. Our findings suggest that xNP1 is involved in both acute phase responses and neural development/functions, which is unique compared to mammalian pentraxins whose family members are specialized in either acute phase responses or neural functions.

First-principles study of spin-wave dispersion in Sm(Fe1-xCox)12

Abstract We present spin-wave dispersion in Sm(Fe1−xCox)12 calculated from first-principles. Anisotropy in the lowest branch of the spin-wave dispersion around the Γ point is discussed. It is shown that spin-waves propagate more easily along a ∗ -axis than along c ∗ -axis, especially in SmFe12. We also compare values of the spin-wave stiffness with those obtained from an experiment. The calculated values are in good agreement with the experimental values.

interleukin-11 induces and maintains progenitors of different cell lineages during Xenopus tadpole tail regeneration

Unlike mammals, Xenopus laevis tadpoles possess high ability to regenerate their lost organs. In amphibians, the main source of regenerated tissues is lineage-restricted tissue stem cells, but the mechanisms underlying induction, maintenance and differentiation of these stem/progenitor cells in the regenerating organs are poorly understood. We previously reported that interleukin-11 (il-11) is highly expressed in the proliferating cells of regenerating Xenopus tadpole tails. Here, we show that il-11 knockdown (KD) shortens the regenerated tail length, and the phenotype is rescued by forced-il-11-expression in the KD tadpoles. Moreover, marker genes for undifferentiated notochord, muscle, and sensory neurons are downregulated in the KD tadpoles, and the forced-il-11-expression in intact tadpole tails induces expression of these marker genes. Our findings demonstrate that il-11 is necessary for organ regeneration, and suggest that IL-11 plays a key role in the induction and maintenance of undifferentiated progenitors across cell lineages during Xenopus tail regeneration.Xenopus laevis tadpoles have maintained their ability to regenerate various organs. Here, the authors show that interleukin-11 is necessary for organ regeneration, by inducing and maintaining undifferentiated progenitors across cell lineages during Xenopus tail regeneration.

Phyhd1, an XPhyH-like homologue, is induced in mouse T cells upon T cell stimulation.

We previously identified XPhyH-like as a gene whose expression is enhanced in Xenopus blood cells during the refractory period, in which Xenopus tadpoles transiently lose their tail regenerative ability. Although we hypothesized that some autoreactive immune cells attack tail blastemal cells during the refractory period and XPhyH-like expressing immune cells were involved in the process, the nature of cells expressing XPhyH-like remain unknown, partly due to the lack of leukocyte markers available in Xenopus. In the present study, we used mice to analyze the expression pattern of XPhyH-like homologues. When we used quantitative reverse transcription-polymerase chain reaction (RT--PCR) to analyze the expression of mouse Phyhd1, an XPhyH-like orthologue, and Phyh, a Phyhd1 paralogue, both Phyhd1 and Phyh showed similar tissue-specific expression patterns. The expression pattern in leukocytes, however, differed between Phyhd1 and Phyh; Phyhd1 was considerably expressed in T cells and B cells. Moreover, the expression of Phyhd1 in T cells was up-regulated for approximately 3- to 7-times by T cell stimulation 3-4 days after the stimulation, unlike Phyh. Our findings suggest that Phyhd1 and Phyh have distinct roles in mouse leukocytes and Phyhd1 is related to T cell differentiation and/or function of effector T cells.