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  • 1
    Publication Date: 2012-03-09
    Description: One of the fascinating aspects of the history of life is the apparent increase in morphological complexity through time, a well known example being mammalian cheek tooth evolution. In contrast, experimental studies of development more readily show a decrease in complexity, again well exemplified by mammalian teeth, in which tooth crown features called cusps are frequently lost in mutant and transgenic mice. Here we report that mouse tooth complexity can be increased substantially by adjusting multiple signalling pathways simultaneously. We cultured teeth in vitro and adjusted ectodysplasin (EDA), activin A and sonic hedgehog (SHH) pathways, all of which are individually required for normal tooth development. We quantified tooth complexity using the number of cusps and a topographic measure of surface complexity. The results show that whereas activation of EDA and activin A signalling, and inhibition of SHH signalling, individually cause subtle to moderate increases in complexity, cusp number is doubled when all three pathways are adjusted in unison. Furthermore, the increase in cusp number does not result from an increase in tooth size, but from an altered primary patterning phase of development. The combination of a lack of complex mutants, the paucity of natural variants with complex phenotypes, and our results of greatly increased dental complexity using multiple pathways, suggests that an increase may be inherently different from a decrease in phenotypic complexity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harjunmaa, Enni -- Kallonen, Aki -- Voutilainen, Maria -- Hamalainen, Keijo -- Mikkola, Marja L -- Jernvall, Jukka -- England -- Nature. 2012 Mar 7;483(7389):324-7. doi: 10.1038/nature10876.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Program, Institute of Biotechnology, University of Helsinki, P.O. Box 56, FIN-00014 Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22398444" target="_blank"〉PubMed〈/a〉
    Keywords: Activins/metabolism/pharmacology ; Animals ; *Biological Evolution ; Developmental Biology ; Ectodysplasins/metabolism/pharmacology ; Hedgehog Proteins/metabolism/pharmacology ; Mice ; Molar/*anatomy & histology/drug effects/embryology/*metabolism ; Mutation ; Organ Culture Techniques ; Phenotype ; *Signal Transduction/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2014-08-01
    Description: The evolutionary relationships of extinct species are ascertained primarily through the analysis of morphological characters. Character inter-dependencies can have a substantial effect on evolutionary interpretations, but the developmental underpinnings of character inter-dependence remain obscure because experiments frequently do not provide detailed resolution of morphological characters. Here we show experimentally and computationally how gradual modification of development differentially affects characters in the mouse dentition. We found that intermediate phenotypes could be produced by gradually adding ectodysplasin A (EDA) protein in culture to tooth explants carrying a null mutation in the tooth-patterning gene Eda. By identifying development-based character inter-dependencies, we show how to predict morphological patterns of teeth among mammalian species. Finally, in vivo inhibition of sonic hedgehog signalling in Eda null teeth enabled us to reproduce characters deep in the rodent ancestry. Taken together, evolutionarily informative transitions can be experimentally reproduced, thereby providing development-based expectations for character-state transitions used in evolutionary studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252015/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252015/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harjunmaa, Enni -- Seidel, Kerstin -- Hakkinen, Teemu -- Renvoise, Elodie -- Corfe, Ian J -- Kallonen, Aki -- Zhang, Zhao-Qun -- Evans, Alistair R -- Mikkola, Marja L -- Salazar-Ciudad, Isaac -- Klein, Ophir D -- Jernvall, Jukka -- DP2 OD007191/OD/NIH HHS/ -- DP2-OD007191/OD/NIH HHS/ -- K99 DE024214/DE/NIDCR NIH HHS/ -- R01 DE021420/DE/NIDCR NIH HHS/ -- R01-DE021420/DE/NIDCR NIH HHS/ -- England -- Nature. 2014 Aug 7;512(7512):44-8. doi: 10.1038/nature13613. Epub 2014 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Biology Program, Institute of Biotechnology, University of Helsinki, P.O. Box 56, FIN-00014 Helsinki, Finland. ; 1] Program in Craniofacial and Mesenchymal Biology, University of California, San Francisco, San Francisco, California 94114, USA [2] Department of Orofacial Sciences, University of California, San Francisco, San Francisco, California 94114, USA. ; Division of Materials Physics, Department of Physics, University of Helsinki, P.O. Box 64, FIN-00014 Helsinki, Finland. ; Key Laboratory of Evolutionary Systematics of Vertebrates, Institute of Vertebrate Paleontology and Paleoanthropology, Chinese Academy of Sciences, Beijing 100044, China. ; 1] School of Biological Sciences, Monash University, Victoria 3800, Australia [2] Geosciences, Museum Victoria, GPO Box 666, Melbourne, Victoria 3001, Australia. ; 1] Developmental Biology Program, Institute of Biotechnology, University of Helsinki, P.O. Box 56, FIN-00014 Helsinki, Finland [2] Genomics, Bioinformatics and Evolution Group. Department de Genetica i Microbiologia, Universitat Autonoma de Barcelona, Cerdanyola del Valles 08193, Spain. ; 1] Program in Craniofacial and Mesenchymal Biology, University of California, San Francisco, San Francisco, California 94114, USA [2] Department of Orofacial Sciences, University of California, San Francisco, San Francisco, California 94114, USA [3] Department of Pediatrics, University of California, San Francisco, San Francisco, California 94114, USA [4] Institute for Human Genetics, University of California, San Francisco, San Francisco, California 94114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25079326" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Computer Simulation ; Ectodysplasins/deficiency/genetics/pharmacology ; Female ; *Fossils ; Gene Deletion ; Hedgehog Proteins/antagonists & inhibitors/genetics ; In Vitro Techniques ; Male ; Mice ; Molar/anatomy & histology/drug effects/growth & development ; Phenotype ; Signal Transduction/drug effects ; Tooth/*anatomy & histology/drug effects/*growth & development
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
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