Unser Haushund: Eine Spitzmaus im Wolfspelz? - Wolf-Ekkehard ...

336Speothos scheint in dieser Frage überhaupt alle Rekorde zu brechen: Nicht nur ist der m2metaconid "greatly reduced or lost", sondern auch m1 metaconid and entoconid 659 sind"greatly reduced or absent", ebenso m2 metaconid and entoconid und die M1-2 hypocones.Auch ist das M1-2 buccal cingulum "reduced or lost".Davon unabhängig sind bei Cuon und Lycaon m2 metaconid and entoconid "greatly reducedor absent" und ebenso die M1-2 hypocones und das M1-2 buccal cingulum ist "reduced orlost".Wie oben schon erwähnt, sind sowohl bei den Caninae (Leptocyon, Vulpini und Canini, mitden Ausnahmen ["Reversals"] von Lycaon und Cuon) die bei den Hesperocyoninae undBorophaginae vorhandenen P3 and p2-3 posterior cusplets "weak or absent." Und die I1-medial cusplets – vorhanden bei den Hesperocyoninae, Borophaginae und Leptocyon (Caninae)– sind "weak or absent" bei den übrigen Caninae.Harjunmaa et al. führen weiter aus, dass die Beobachtungen beim Menschen mitden Forschungsergebnissen bei Mäusen übereinstimmen (p. 324):"Furthermore, both syndromic and normal variation in human dentition predominantly causesimplification or complete loss of teeth 660 , agreeing with the data from mice but contrasting with themacroevolutionary patterns. The prevalence of simple mutants is perhaps to be expected because mostmutations may compromise individual signalling pathways required for organ development.Furthermore, the lack of complex mutants could be due to the relatively few gain-of-function mutationsstudied, or few mutations in feedback inhibitors of major signalling pathways (Supplementary Table 1).This missing 'complexity gene' scenario, however, is not the only plausible hypothesis because asubstantial increase in complexity can also be proposed to require simultaneous changes in severalsignalling pathways (or multiple changes in a single pathway). This requirement of multiple changes canbe conceptualized as 'economics of signalling' in which, for example, increasing signalling through onepathway alone may deplete other signals required to produce a greater number of cusps. In genetic terms,this would approximate a polygenic effect.”"…a substantial increase in complexity can also be proposed to requiresimultaneous changes in several signalling pathways (or multiple changes in asingle pathway)": Das ist im Prinzip der Kernpunkt, den die mit Sachargumentenarbeitenden Kritiker des Darwinismus und der Synthetischen Evolutionstheorie(Neodarwinismus, Gradualismus) seit Jahrzehnten, wenn nicht schon seit mehr als140 Jahren (spätestens mit der Arbeit On the Genesis of Species 661 (1871) von St.George Jackson Mivart 662 ) immer wieder betont haben. Beispiel Auge:Bei dem Koadaptationsproblem müssten zahlreiche richtungslose Mutationen an einer Ketteverschiedener Punkte (den zahlreichen Strukturen im Auge, Sehnerv, Chiasma opticum, Gehirn, Muskelnetc.) gleichzeitig und gleichsinnig, im genau passender Richtung, ansetzen. Wir finden hier einevielfache Koadaptation: einmal bei den inneren und äußeren Strukturen des Auges selbst, dann in der659 Entoconid: "the posterointernal cusp of the talon of a lower molar tooth” http://www.merriam-webster.com/medical/entoconid660 "In humans, inherited variation in the number, size, and shape of teeth within the dentitions are relatively common, while rarer defects of hard tissueformation, including amelogenesis and dentinogenesis imperfecta, and problems associated with tooth eruption are also seen. In many cases, theseanomalies occur in isolation, but they can also present as a feature of numerous well-characterized developmental syndromes. Complex reiterativesignaling between the epithelium and mesenchyme is a feature of normal tooth development in the embryo, occurring from early patterning throughmorphogenesis, hard tissue formation and during root development. Significant events also occur during postnatal development of the dentition, includinghard tissue maturation and tooth eruption. In the last decade, advances in human and mouse genetics have meant that in many cases candidate geneshave been identified for these anomalies. These genes have provided a useful platform for developmental biologists, allowing them to begin elucidatinghow these signals interact to generate a functional dentition and understand the mechanisms underlying many of the anomalies that are seen in humanpopulations.” – Martyn T. Cobourne, Paul T. Sharpe (2012): Diseases of the tooth: the genetic and molecular basis of inherited anomalies affecting thedentition. (2013:WIREs Developmental Biology 2: 183-212)http://wires.wiley.com/WileyCDA/WiresArticle/articles.html?doi=10.1002%2Fwdev.66.Vgl. auch http://www.icd10data.com/ICD10CM/Codes/K00-K95/K00-K14/K00-/K00.2 (2013); http://ghr.nlm.nih.gov/condition/amelogenesis-imperfecta(2007/2013).Ein paar Punkte zum Haushund hier: http://www.mudicompass.org/teethandbite.html und hier: http://actavet.vfu.cz/pdf/200170010065.pdf (P. 69: "Thedog probably suffers from more hereditary dental abnormalities than any other animal, because of the difference in size and shape of breeds as wellas from intensive and sometimes indiscriminate inbreeding (Kertesz 1993)”.)661 http://www.archive.org/stream/genesisofspecies00miva#page/n7/mode/2up662 https://en.wikipedia.org/wiki/St._George_Jackson_Mivart