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      Where did bone come from? : An overview of its evolution

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      1 , , 2
      Acta Orthopaedica
      Informa Healthcare

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          Abstract

          Bone is specific to vertebrates, and originated as mineralization around the basal membrane of the throat or skin, giving rise to tooth-like structures and protective shields in animals with a soft cartilage-like endoskeleton. A combination of fossil anatomy and genetic information from modern species has improved our understanding of the evolution of bone. Thus, even in man, there are still similarities in the molecular regulation of skin appendages and bone. This article gives a brief overview of the major milestones in skeletal evolution. Some molecular machineries involving members of core genetic networks and their interactions are described in the context of both old theories and modern genetic approaches.

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          Most cited references47

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          Buried alive: how osteoblasts become osteocytes.

          During osteogenesis, osteoblasts lay down osteoid and transform into osteocytes embedded in mineralized bone matrix. Despite the fact that osteocytes are the most abundant cellular component of bone, little is known about the process of osteoblast-to-osteocyte transformation. What is known is that osteoblasts undergo a number of changes during this transformation, yet retain their connections to preosteoblasts and osteocytes. This review explores the osteoblast-to-osteocyte transformation during intramembranous ossification from both morphological and molecular perspectives. We investigate how these data support five schemes that describe how an osteoblast could become entrapped in the bone matrix (in mammals) and suggest one of the five scenarios that best fits as a model. Those osteoblasts on the bone surface that are destined for burial and destined to become osteocytes slow down matrix production compared to neighbouring osteoblasts, which continue to produce bone matrix. That is, cells that continue to produce matrix actively bury cells producing less or no new bone matrix (passive burial). We summarize which morphological and molecular changes could be used as characters (or markers) to follow the transformation process. 2005 Wiley-Liss, Inc.
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            Runx2 and Runx3 are essential for chondrocyte maturation, and Runx2 regulates limb growth through induction of Indian hedgehog.

            The differentiation of mesenchymal cells into chondrocytes and chondrocyte proliferation and maturation are fundamental steps in skeletal development. Runx2 is essential for osteoblast differentiation and is involved in chondrocyte maturation. Although chondrocyte maturation is delayed in Runx2-deficient (Runx2(-/-)) mice, terminal differentiation of chondrocytes does occur, indicating that additional factors are involved in chondrocyte maturation. We investigated the involvement of Runx3 in chondrocyte differentiation by generating Runx2-and-Runx3-deficient (Runx2(-/-)3(-/-)) mice. We found that chondrocyte differentiation was inhibited depending on the dosages of Runx2 and Runx3, and Runx2(-/-)3(-/-) mice showed a complete absence of chondrocyte maturation. Further, the length of the limbs was reduced depending on the dosages of Runx2 and Runx3, due to reduced and disorganized chondrocyte proliferation and reduced cell size in the diaphyses. Runx2(-/-)3(-/-) mice did not express Ihh, which regulates chondrocyte proliferation and maturation. Adenoviral introduction of Runx2 in Runx2(-/-) chondrocyte cultures strongly induced Ihh expression. Moreover, Runx2 directly bound to the promoter region of the Ihh gene and strongly induced expression of the reporter gene driven by the Ihh promoter. These findings demonstrate that Runx2 and Runx3 are essential for chondrocyte maturation and that Runx2 regulates limb growth by organizing chondrocyte maturation and proliferation through the induction of Ihh expression.
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              The evolution of hierarchical gene regulatory networks.

              Comparative developmental evidence indicates that reorganizations in developmental gene regulatory networks (GRNs) underlie evolutionary changes in animal morphology, including body plans. We argue here that the nature of the evolutionary alterations that arise from regulatory changes depends on the hierarchical position of the change within a GRN. This concept cannot be accomodated by microevolutionary nor macroevolutionary theory. It will soon be possible to investigate these ideas experimentally, by assessing the effects of GRN changes on morphological evolution.
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                Author and article information

                Journal
                Acta Orthop
                ORT
                Acta Orthopaedica
                Informa Healthcare
                1745-3674
                1745-3682
                August 2011
                02 September 2011
                : 82
                : 4
                : 393-398
                Affiliations
                1simpleInstitute of Chemistry and Biochemistry , Freie Universität Berlin, Berlin, Germany
                2Orthopedics, AIR/IKE, Faculty of Health Science, Linköping University, Linköping, Sweden
                Correspondence: darja_obradovic@ 123456yahoo.de
                Article
                ORT_A_588861_O
                10.3109/17453674.2011.588861
                3237026
                21657973
                a1312213-9782-4900-87e2-55dcdf826edc
                Copyright: © Nordic Orthopaedic Federation

                This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited.

                History
                : 07 December 2010
                : 08 March 2011
                Categories
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                Orthopedics
                Orthopedics

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