Mutations affecting segment number and polarity in Drosophila

Nüsslein‐Volhard, Christiane; Wieschaus, Eric

doi:10.1038/287795a0

Cited by 3,874 publications

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“…Hedgehog was identified in genetic screens in Drosophila in 1980, and the vertebrate hedgehog proteins were discovered in 1993 (Krauss et al, 1993; Nusslein-Volhard and Wieschaus, 1980). Since then, investigations on the role of hedgehog signaling in organ development and diseases progression have rapidly accelerated.…”

Section: Introductionmentioning

confidence: 99%

Sonic hedgehog signaling in kidney fibrosis: a master communicator

Zhou

Tan

Liu

2016

Sci. China Life Sci.

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The hedgehog signaling cascade is an evolutionarily conserved pathway that regulates multiple aspects of embryonic development and plays a decisive role in tissue homeostasis. As the best studied member of three hedgehog ligands, sonic hedgehog (Shh) is known to be associated with kidney development and tissue repair after various insults. Recent studies uncover an intrinsic link between dysregulated Shh signaling and renal fibrogenesis. In various types of chronic kidney disease (CKD), Shh is upregulated specifically in renal tubular epithelium but targets interstitial fibroblasts, thereby mediating a dynamic epithelial-mesenchymal communication (EMC). Tubule-derived Shh acts as a growth factor for interstitial fibroblasts and controls a hierarchy of fibrosis-related genes, which lead to the excessive deposition of extracellular matrix in renal interstitium. In this review, we recapitulate the principle of Shh signaling, its activation and regulation in a variety of kidney diseases. We also discuss the potential mechanisms by which Shh promotes renal fibrosis and assess the efficacy of blocking this signaling in preclinical settings. Continuing these lines of investigations will provide novel opportunities for designing effective therapies to improve CKD prognosis in patients.

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Section: Introductionmentioning

confidence: 99%

Sonic hedgehog signaling in kidney fibrosis: a master communicator

Zhou

Tan

Liu

2016

Sci. China Life Sci.

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“…The hedgehog (Hh) gene was identified in 1980 through genetic analysis of segmentation of fruit fly Drosophila (Nusslein-Volhard and Wieschaus, 1980). In the early 1990s, three homologs of the Hh gene were identified in vertebrates (Echelard et al, 1993;Krauss et al, 1993;Riddle et al, 1993;Chang et al, 1994;Roelink et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Activation of the hedgehog-signaling pathway in human cancer and the clinical implications

et al. 2009

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“…During the 1980s, researchers screened thousands of fly mutants created in large-scale mutagenesis experiments. These screens revealed only a small number of variants in segment number, orientation, and identity [21]. Among these variants were embryos that lacked several consecutive segments and embryos that lacked every other (odd-numbered or even-numbered) segment.…”

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confidence: 99%

Genotype networks shed light on evolutionary constraints

Wagner

2011

Trends in Ecology & Evolution

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An evolutionary constraint is a bias or limitation in phenotypic variation that a biological system produces. One can distinguish physicochemical, selective, genetic and developmental causes of such constraints. Here, I discuss these causes in three classes of system that bring forth many phenotypic traits and evolutionary innovations: regulatory circuits, macromolecules and metabolic networks. In these systems, genotypes with the same phenotype form large genotype networks that extend throughout a vast genotype space. Such genotype networks can help unify different causes of evolutionary constraints. They can show that these causes ultimately emerge from the process of development; that is, how phenotypes form from genotypes. Furthermore, they can explain important consequences of constraints, such as punctuated stasis and canalization. An evolutionary constraint is a bias or limitation in phenotypic variation that a biological system produces. One can distinguish physicochemical, selective, genetic and developmental causes of such constraints. Here, I discuss these causes in three classes of systems that bring forth many phenotypic traits and evolutionary innovations: regulatory circuits, macromolecules and metabolic networks. In these systems, genotypes with the same phenotype form large genotype networks that extend throughout a vast genotype space. Such genotype networks can help unify different causes of evolutionary constraints. They can show that these causes ultimately emerge from the process of development: that is, how phenotypes form from genotypes. Furthermore, they can explain important consequences of constraints, such as punctuated stasis and canalization. Evolutionary constraintsNo organism or species can produce every conceivable kind of phenotypic variation. This limitation is encapsulated in the notion of constraints on phenotypic evolution [1]. An evolutionary constraint is a bias or limitation in phenotypic variation that a biological system produces. Extreme examples include the absence of photosynthesis in higher animals, the general lack of teeth in the lower jaw of frogs, the absence of palm trees in cold climates and the absence of birds that give birth to live young instead of to eggs [1,2]. In these examples, a trait is completely absent. More subtle constraints manifest themselves as correlations among different characters. A paradigmatic case is allometric scaling [2]. Here, the value of one quantitative trait constrains that of another, typically via a specific nonlinear relationship, For example, metabolic rate is proportional to body mass m raised to approximately three quarter power (m 0.75 ) across many differentIt is not hard to see that constraints can influence the spectrum of evolutionary adaptations and innovations that are accessible to living things. For this reason, questions about the causes and consequences of constrained evolution have attracted much attention [1,[4][5][6][7][8][9][10]. There are multiple kinds and causes of phenotypic constraints (Box 1),...

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Mutations affecting segment number and polarity in Drosophila

Cited by 3,874 publications

References 13 publications

Sonic hedgehog signaling in kidney fibrosis: a master communicator

Sonic hedgehog signaling in kidney fibrosis: a master communicator

Activation of the hedgehog-signaling pathway in human cancer and the clinical implications

Genotype networks shed light on evolutionary constraints

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