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Title: Transient laminin beta 1a Induction Defines the Wound Epidermis during Zebrafish Fin Regeneration}
Article:
Abstract:
The first critical stage in salamander or teleost appendage regeneration is creation of a specialized epidermis that instructs growth from underlying stump tissue. Here, we performed a forward genetic screen for mutations that impair this process in amputated zebrafish fins. Positional cloning and complementation assays identified a temperature-sensitive allele of the ECM component laminin beta 1a( lamb1a) that blocks fin regeneration. lamb1a, but not its paralog lamb1b, is sharply induced in a subset of epithelial cells after fin amputation, where it is required to establish and maintain a polarized basal epithelial cell layer. These events facilitate expression of the morphogenetic factors shha and lef1, basolateral positioning of phosphorylated Igf1r, patterning of new osteoblasts, and regeneration of bone. By contrast, lamb1a function is dispensable for juvenile body growth, homeostatic adult tissue maintenance, repair of split fins, or renewal of genetically ablated osteoblasts. fgf20a mutations or transgenic Fgf receptor inhibition disrupt lamb1a expression, linking a central growth factor to epithelial maturation during regeneration. Our findings reveal transient induction of lamb1a in epithelial cells as a key, growth factor-guided step in formation of a signaling-competent regeneration epidermis.
Introduction:
Mammals have a limited ability to regenerate complex structures like limbs, heart or central nervous system tissue. By contrast, teleost fish and urodele amphibians can regenerate major appendages, spinal cord, retina, brain, kidney, and the heart[1–7]. How and why tissue regeneration occurs in non-mammalian vertebrates has fascinated biologists for centuries and is relevant to regenerative medicine strategies. Previous studies of appendage regeneration have identified three prominent phases: 1) wound healing; 2) blastema formation; and 3) regenerative outgrowth and patterning[8]. Upon amputation injury, the exposed stump tissue is rapidly covered by a sheet of epithelial cells, a process involving little or no cell proliferation[9, 10]. Classical studies in salamanders revealed that if this epithelium is removed, replaced with flank skin, or disrupted by insertion of the limb into the abdominal cavity, limb regeneration does not proceed[11–13]. The wound epithelium becomes multilayered and acquires a layer of cuboidal basal epithelial cells over the next hours to days, maturing into a structure commonly referred to as the wound or regeneration epidermis. Regeneration epidermises of salamander limbs or teleost fins are known to express markers of developmental signaling pathways, including many secreted factors[8, 14]. For instance, after initial epithelialization of an amputated zebrafish fin stump, epithelial and/or mesenchymal cells induce effectors of pathways mediated by Fgfs, Igfs, Wnts, Hhs, Activin-βA/TGFβ, Retinoic acid, Bmps, and Notch[15–27]. Interestingly, fgf20a and igf2b ligand genes are induced within hours of fin amputation in mesenchymal cells, and perturbation of Fgf signaling via a mutation in the fgf20a ligand gene, or of Igf signaling by receptor inhibition, disrupts formation of the regeneration epidermis and subsequent bone regeneration[20, 21]. These findings indicate an important role for early expression of growth factors in structural and functional maturation of epithelial tissue. However, mechanisms by which these pathways define the morphology and signaling activities of the regeneration epidermis have not been addressed. Here, we used forward genetics to identify a critical role for laminin beta 1a( lamb1a), one of two paralogs encoding a Laminin beta 1 extracellular matrix component, in zebrafish fin regeneration. lamb1a is sharply induced upon fin amputation in the basal layer of the wound epithelium, where its function is required to establish polarity in basal epithelial cells, induce and maintain basal epithelial markers, localize receptors for signaling, and align regenerating osteoblasts. lamb1a induction is dependent on Fgf signaling, both immediately after amputation and throughout regeneration. Thus, Lamb1a is a critical node between growth factor signals and formation of the regeneration epidermis in an amputated vertebrate appendage.
Discussion:
Here, we carried out a forward genetic screen for zebrafish mutants defective in creation of a signaling-competent regeneration epidermis. The sde1 product is not required to repopulate genetically ablated osteoblasts or heal incision wounds, and appears largely dispensable in uninjured adult animals. However, after fin amputation, sde1 lesions disrupt epidermal maturation and signaling, and impair osteoblast patterning, and they remain inhibitory throughout the process of tissue replacement. Genetic analyses, including gene product assessment and complementation with known mutants, define sde1 as a temperature-sensitive allele of lamb1a, an ECM component that is transiently induced by injury in a subset of epithelial cells. Thus, Lamb1a is a key component of the regeneration epidermis with context-specific roles in appendage regeneration. Our findings, combined with those of past studies, suggest a regulatory model for construction and maintenance of the regeneration epidermis( Fig 8). After an amputation injury, the wound closes within the next several hours by epithelial cell migration, ostensibly controlled by tension changes within the epithelial sheet. fgf20a is induced at the epithelial-mesenchymal boundary by 6 hours post-amputation. One direct or indirect function of fgf20a signaling is to induce expression of the lamb1a paralog in the adjacent epithelial cell layer, which establishes a basement membrane and polarizes the basal cell layer. This polarization is essential for positioning signaling receptors, such as phosphorylated Igf1r, and induction of factors involved in Hh signaling and Wnt/β-catenin signaling( via indirect influences[17, 49]) that guide osteoblast patterning and bone formation. During regenerative outgrowth, Fgf signaling retains lamb1a expression in the basal cell layer, maintaining polarization in basal epithelial cells and the competence to signal to osteoblasts. Our results with FK506 indicate that Lamb1a function is predominantly epithelial, as activation of the mesenchymal component is sufficient to promote bone regeneration to a certain degree even in the presence of a disrupted regeneration epidermis. Fgf ligand presence and Lamb1a expression wane after completion of regeneration[48]. ECM components have been implicated in tissue regeneration in several recent studies, including tadpole tail bud regeneration, zebrafish heart regeneration, and newt heart regeneration[50–52]. It is generally challenging to dissect their biological functions during regeneration, as Laminins and other ECM molecules are often required during embryogenesis. For example, mice with null mutations in Lama1, Lamb1, or Lamc1, and zebrafish with mutations in lamb1a, lama5, or several other ECM components[41, 42, 53–55], each die at embryonic stages. However, as we reveal here, the regulation of Laminin is also critical in the context of regenerating large regions of bone, in a way we expect is both structurally to create an epidermal scaffold and chemically as a source of signaling factors. While our data implicate fgf20a as an inducer of lamb1a during fin regeneration, there may exist other regulatory inputs for this and distinct ECM factors. For example, Nagendran and colleagues recently reported in a morpholino-based study that lama5 expression is under control of canonical Wnt signaling in the embryonic zebrafish fin epithelium[56]. Thus, it is possible that the regeneration epidermis is shaped by a network of growth factor-ECM regulatory interactions. Interestingly, the estimated timing of teleost genome duplication precedes the dramatic rise of biological diversification in teleosts, according to paleontological evidence[38]. This is consistent with the hypothesis that gene duplication offers surplus genetic materials as origins of new biological functions. Recently, Rohner and colleagues reported that either of the two fibroblast growth factor receptor 1 paralogs( fgfr1a and fgfr1b) is sufficient for embryogenesis in zebrafish, whereas loss-of-function in both paralogs is lethal[57]. Only one of the paralogs, fgfr1a, is specifically expressed in the skin of 30 day-old juveniles, where its function is required for normal adult scale development in adult zebrafish and carp. Here, we found that lamb1a, but not lamb1b, is induced during fin regeneration, where it is essential. We speculate that maintenance of two lamb1 paralogs preserved viability in the setting of new mutations, permitting selection events that were favorable to adult regenerative potential. Comparison of the regulatory sequences of the lamb1 paralogs, and other sets of paralogs with similar divergent expression upon injury, could help decode genetic modifications that have preserved or dampened regenerative capacity in the evolution of vertebrate species.
Unlike mammals , adult teleost fish and urodele amphibians can fully regenerate lost appendages . Understanding what initiates regeneration in these vertebrates is of great interest to the scientific community . It has long been known that the epidermis that forms quickly over an amputated limb stump is critical for initiating regenerative programs . Yet , little of understood of the molecular and cellular mechanisms by which a simple adult epithelium transforms into this key signaling source . Here , we performed a large-scale , unbiased genetic screen for epithelial signaling deficiencies during the regeneration of amputated adult zebrafish fins , from which we identified several new mutants . One gene identified from this screen disrupts a specific component of the extracellular matrix material Laminin , Laminin beta 1a , a factor that we find to be dispensable in uninjured adult animals but required for all stages fin regeneration . Transient induction of this component by amputation polarizes the basal layer of the nascent epithelium , and , in turn , facilitates the synthesis of signaling factors , the positioning of ligand receptors , and the patterning of new bone cells . We also find that normal induction of Laminin beta 1a by injury relies on the function of Fibroblast growth factors , secreted polypeptide signals that are released early upon injury . Our results identify key early steps in the endogenous program for vertebrate appendage regeneration .