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A paradigm for thinking about wholes, their constitution and re-production, has long been provided by living organisms. While the emphasis is often on the relation between parts and wholes - between the functionally differentiated organs and the organism, or, on a lower level, between cells and organs - Robert Meunier and Valentine Reynaud's essay 'The Innate Plasticity of Bodies and Minds: Integrating Models of Genetic Determination and Environmental Formation' poses the question of the whole in biology with respect to the organism and its environment. A developmental system involves not only what we conventionally discern as the organism, that is, initially, the fertilized egg and the cellular mass arising from it by cell division, but also the physical and biological surrounding of the developing embryo. In the sense that not every aspect of the environment plays a role, the organism as part of the system constitutes this whole by determining what has an effect on the process and what does not. On the other hand, by not only enabling development or providing material but instead shaping the process in specific ways, the whole of organism-environment interactions constitutes its part, i.e., the developing organism. If there are therefore different, potentially incommensurable constitutions of the whole developmental system, there are also different ways of identifying the relevant units of selection in evolution, such as the living organism as a whole or the genes as the units of replication. In their essay, Meunier and Reynaud argue for a view on development and evolution that integrates notions of environmental influence and genetic determination. The notion of plasticity that has recently gained currency in the life sciences seems to oppose genetic determination and innateness by underlining the importance of environmental influence. However, while morphological and cognitive development is indeed plastic and sensitive to the environment, the essay emphasizes that the mechanisms and elements enabling a system to respond to influences must be available for development to happen in the first place. These resources for development are not homogeneous 'stuff' that becomes formed by the environment through the course of development. Instead, they are highly structured and specific and thus enable specific responses to contextual conditions. Under varying conditions they will of course appear in different combinations and produce different outcomes. Thus, they enable plasticity. And yet, as they are specific mechanisms and elements, which mainly gain their specificity from the structure of the genetic material on which the environment can act, it appears appropriate to refer to them as innate.
Latent TGF-β binding protein 2 and 4 have essential overlapping functions in microfibril development
(2017)
Microfibrils are exracellular matrix components necessary for elastic fiber assembly and for suspending lenses. We previously reported that latent TGF-β binding protein 2 (LTBP-2), a microfibril-associated protein, is required for forming stable microfibril bundles in ciliary zonules. However, it was not understood why Ltbp2 null mice only showed an eye-specific phenotype, whereas LTBP-2 is abundantly expressed in other tissues containing microfibrils in wild type mice. Here, we show that LTBP-4, another microfibril-associated protein, compensates for the loss of LTBP-2 in microfibril formation. Ltbp2/4S double knockout (DKO) mice showed increased lethality due to emphysema, which was much more severe than that found in Ltbp4S null mice. Elastic fibers in the lungs of Ltbp2/4S DKO mice were severely disorganized and fragmented. Cultured mouse embryonic fibroblasts (MEFs) from Ltbp2/4S DKO embryos developed reduced microfibril meshwork in serum-free conditions, whereas the microfibril formation was restored by the addition of either recombinant LTBP-2 or -4. Finally, ectopic expression of LTBP-4 in the whole body restored ciliary zonule microfibril bundles in the eyes of Ltbp2 null mice. These data suggest that LTBP-2 and -4 have critical overlapping functions in forming the robust structure of microfibrils in vitro and in vivo.