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Audio versions of bioRxiv paper abstracts

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Audio versions of bioRxiv paper abstracts

    Molluscan dorsal-ventral patterning relying on BMP24 and Chordin provides insights into spiralian development and bilaterian body plan evolution

    Molluscan dorsal-ventral patterning relying on BMP24 and Chordin provides insights into spiralian development and bilaterian body plan evolution

    Link to bioRxiv paper:
    http://biorxiv.org/cgi/content/short/2020.08.11.245670v1?rss=1

    Authors: Tan, S., Huan, P., Liu, B.

    Abstract:
    The molecular mechanisms of dorsal-ventral (DV) patterning in Spiralia are poorly understood. The few available studies indicate that derived DV patterning mechanisms occurred in particular spiralian lineages and likely were related to the loss of Chordin gene. Here, a functional study of the first spiralian Chordin showed that BMP2/4 and Chordin regulate DV patterning in the mollusk Lottia goshimai, thus revealing the first spiralian case that retains this conserved mechanism. We then showed that Chordin but not BMP2/4 transferred the positional information of the D-quadrant organizer to establish the BMP signaling gradient along the presumed DV axis. Further investigations on the molluscan embryos with influenced DV patterning suggested a role of BMP signaling in regulating the organization of the larval nervous system and indicated that the blastopore localization is correlated with the BMP signaling gradient. These findings provide insights into the evolution of animal DV patterning, the unique development mode of spiralians driven by the D-quadrant organizer, and the evolution of bilaterian body plans.

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    Timed mesodermal FGF and BMP govern the multi-step thyroid specification

    Timed mesodermal FGF and BMP govern the multi-step thyroid specification

    Link to bioRxiv paper:
    http://biorxiv.org/cgi/content/short/2020.08.13.249540v1?rss=1

    Authors: Haerlingen, B., Opitz, R., Vandernoot, I., Molinaro, A., Shankar, M., Gillotay, P., Trubiroha, A., Costagliola, S.

    Abstract:
    The thyroid plays an essential role in homeostasis and development, but the extrinsic regulation of its embryonic development remains poorly understood. Recently, we have identified the FGF and BMP pathways to be crucial for thyroid specification and have confirmed the hypothesis that the cardiac mesoderm provides the FGF and BMP ligands to regulate this process. However, it is not clear how these ligands control thyroid specification. To study the molecular mechanisms underlying early thyroid development, we combined a pharmacological approach in zebrafish embryos with genetic models, to modulate the activity of the FGF and BMP pathways at different embryonic stages. We first characterized the expression of the transcription factors pax2a and nkx2.4b - the two main early thyroid markers - in the anterior foregut endoderm and observed that pax2a was expressed from 18 hours post fertilization (hpf) and marked a large endodermal cell population while nkx2.4b was expressed from 24 hpf and marked only a subset of the pax2a-positive endodermal cells. Interestingly, the activity profiles of FGF and BMP coincided with the detection of pax2a and nkx2.4b expression, respectively. Brief modulations of the FGF and/or BMP pathways support the hypothesis that the FGF pathway regulates the expression of pax2a and the BMP pathway regulates the expression of nkx2.4b. Furthermore, inhibition of the BMP pathway during early segmentation has dramatic effects on thyroid specification, probably via the FGF pathway. Together with our previous observations, we propose here, an updated model of early thyroid development in which the foregut endoderm receives several synchronized waves of FGF and BMP signals from the cardiac mesoderm, which result in sequential activation of pax2a and nkx2.4b gene expression and subsequent thyroid specification

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    Regulated delivery controls Drosophila Hedgehog, Wingless and Decapentaplegic signaling

    Regulated delivery controls Drosophila Hedgehog, Wingless and Decapentaplegic signaling

    Link to bioRxiv paper:
    http://biorxiv.org/cgi/content/short/2020.08.12.247759v1?rss=1

    Authors: Kornberg, T. B., Hatori, R.

    Abstract:
    Morphogen signaling proteins disperse across tissues to activate signal transduction in target cells. We investigated dispersion of Hedgehog (Hh), Wingless (Wg), and Bone morphogenic protein homolog Decapentaplegic (Dpp) in the Drosophila wing imaginal disc, and found that delivery to targets is regulated. Cells take up 5% Hh produced, and neither amounts taken up nor extent of signaling changes under conditions of Hh production from 50-200% normal amounts. Similarly, cells take up 25% Wg produced, and variation in Wg production from 50-700% normal has no effect on amounts taken up or signaling. Similar properties were observed for Dpp. Wing disc-produced Hh signals to disc-associated tracheal and myoblast as well as an approximately equal number of disc cells, but the extent of signaling in the disc is unaffected by the presence or absence of the tracheal cells and myoblasts. These findings show that target cells do not take up signaling proteins from a common pool and that both the amount and destination of delivered morphogens are regulated.

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    FGF signaling induces mesoderm in members of Spiralia

    FGF signaling induces mesoderm in members of Spiralia

    Link to bioRxiv paper:
    http://biorxiv.org/cgi/content/short/2020.08.13.249714v1?rss=1

    Authors: Andrikou, C., Hejnol, A.

    Abstract:
    FGF signaling is involved in mesoderm induction in deuterostomes, but not in flies and nematodes, where it has a role in mesoderm patterning and migration. However, comparable studies in other protostomic taxa are missing in order to decipher whether this mesoderm-inducing function of FGF extends beyond the lineage of deuterostomes. Here, we investigated the role of FGF signaling during mesoderm development in three species of lophophorates, a clade within the protostome group Spiralia. Our gene expression analyses show that the molecular patterning of mesoderm development is overall conserved between brachiopods and phoronids, but the spatial and temporal recruitment of transcription factors differs significantly. Moreover, inhibitor experiments demonstrate that FGF signaling is involved in mesoderm formation, morphogenetic movements of gastrulation and posterior axial elongation. Our findings suggest that the inductive role of FGF in mesoderm possibly predates the origin of deuterostomes.

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    PTEN Inhibition Ameliorates Muscle Degeneration and Improves Muscle Function in a Mouse Model of Duchenne Muscular Dystrophy

    PTEN Inhibition Ameliorates Muscle Degeneration and Improves Muscle Function in a Mouse Model of Duchenne Muscular Dystrophy

    Link to bioRxiv paper:
    http://biorxiv.org/cgi/content/short/2020.08.13.249961v1?rss=1

    Authors: Yue, F., Song, C., Huang, D., Narayanan, N., Qiu, J., Jia, Z., Yuan, Z., Oprescu, S. N., Roseguini, B. T., Deng, M., Kuang, S.

    Abstract:
    Duchenne Muscular Dystrophy (DMD) is caused by mutation of the muscle membrane protein dystrophin and characterized by severe degeneration of myofibers, progressive muscle wasting and loss of mobility, ultimately cardiorespiratory failure and premature death. Here we report that skeletal muscle-specific knockout (KO) of Phosphatase and tensin homolog (Pten) gene in an animal model of DMD (mdx mice) alleviates myofiber degeneration and restores muscle function without increasing tumor incidences. Specifically, Pten KO normalizes myofiber size and prevents muscular atrophy, and improves grip strength and exercise performance of mdx mice. Pten KO also reduces fibrosis and inflammation; and ameliorates muscle pathology in mdx mice. Moreover, we found that Pten KO upregulates extracellular matrix and basement membrane components positively correlated to wound healing, but suppresses negative regulators of wound healing and lipid biosynthesis; and restores the integrity of muscle basement membrane in mdx mice. Importantly, pharmacological inhibition of PTEN similarly ameliorates muscle pathology and improves muscle integrity and function in mdx mice. Our finding provides evidence that PTEN inhibition may represent a potential therapeutic strategy to restore muscle function in DMD.

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    A Wnt-specific astacin proteinase controls head formation in Hydra

    A Wnt-specific astacin proteinase controls head formation in Hydra

    Link to bioRxiv paper:
    http://biorxiv.org/cgi/content/short/2020.08.13.247569v1?rss=1

    Authors: Ziegler, B., Yiallouros, I., Trageser, B., Kumar, S., Mercker, M., Kling, S., Fath, M., Warnken, U., Schnoelzer, M., Holstein, T. W., Hartl, M., Marciniak-Czochra, A., Stetefeld, J., Stoecker, W., Oezbek, S.

    Abstract:
    The Hydra head organizer acts as a signaling center that initiates and maintains the primary body axis in steady state polyps and during budding or regeneration. Wnt/beta-Catenin signaling functions as a primary cue controlling this process, but how Wnt ligand activity is locally restricted at the protein level is poorly understood. Here we report the identification of an astacin family proteinase as a Wnt processing factor. Hydra astacin-7 (HAS-7) is expressed from gland cells as an apical-distal gradient in the body column, peaking close beneath the tentacle zone. HAS-7 siRNA knockdown abrogates HyWnt3 proteolysis in the head tissue and induces a robust double axis phenotype, which is rescued by simultaneous HyWnt3 knockdown. Accordingly, double axes are also observed in conditions of increased Wnt levels as in transgenic actin::HyWnt3 and HyDkk1/2/4 siRNA treated animals. HyWnt3-induced double axes in Xenopus embryos could be rescued by co-injection of HAS-7 mRNA. Mathematical modelling combined with experimental promotor analysis indicate an indirect regulation of HAS-7 by beta-Catenin, expanding the classical Turing-type activator-inhibitor model. Our data suggest a negative regulatory function of Wnt processing astacin proteinases in the global patterning of the oral-aboral axis in Hydra.

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