White Axolotl Research Articles

Mapping hematopoiesis in a fully regenerative vertebrate: the axolotl

AbstractHematopoietic stem cell (HSC)-derived cells are involved in wound healing responses throughout the body. Unfortunately for mammals, wound repair typically results in scarring and nonfunctional reparation. Among vertebrates, none display such an extensive ability for adult regeneration as urodele amphibians, including 1 of the more popular models: the axolotl. However, a lack of knowledge of axolotl hematopoiesis hinders the use of this animal for the study of hematopoietic cells in scar-free wound healing and tissue regeneration. We used white and cytomegalovirus:green fluorescent protein+ transgenic white axolotl strains to map sites of hematopoiesis and develop hematopoietic cell transplant methodology. We also established a fluorescence-activated cell sorter enrichment technique for major blood lineages and colony-forming unit assays for hematopoietic progenitors. The liver and spleen are both active sites of hematopoiesis in adult axolotls and contain transplantable HSCs capable of long-term multilineage blood reconstitution. As in zebrafish, use of the white axolotl mutant allows direct visualization of homing, engraftment, and hematopoiesis in real time. Donor-derived hematopoiesis occurred for >2 years in recipients generating stable hematopoietic chimeras. Organ segregation, made possible by embryonic microsurgeries wherein halves of 2 differently colored embryos were joined, indicate that the spleen is the definitive site of adult hematopoiesis.

Neural Crest Does Not Contribute to the Neck and Shoulder in the Axolotl (Ambystoma mexicanum)

BackgroundA major step during the evolution of tetrapods was their transition from water to land. This process involved the reduction or complete loss of the dermal bones that made up connections to the skull and a concomitant enlargement of the endochondral shoulder girdle. In the mouse the latter is derived from three separate embryonic sources: lateral plate mesoderm, somites, and neural crest. The neural crest was suggested to sustain the muscle attachments. How this complex composition of the endochondral shoulder girdle arose during evolution and whether it is shared by all tetrapods is unknown. Salamanders that lack dermal bone within their shoulder girdle were of special interest for a possible contribution of the neural crest to the endochondral elements and muscle attachment sites, and we therefore studied them in this context.ResultsWe grafted neural crest from GFP+ fluorescent transgenic axolotl (Ambystoma mexicanum) donor embryos into white (d/d) axolotl hosts and followed the presence of neural crest cells within the cartilage of the shoulder girdle and the connective tissue of muscle attachment sites of the neck-shoulder region. Strikingly, neural crest cells did not contribute to any part of the endochondral shoulder girdle or to the connective tissue at muscle attachment sites in axolotl.ConclusionsOur results in axolotl suggest that neural crest does not serve a general function in vertebrate shoulder muscle attachment sites as predicted by the “muscle scaffold theory,” and that it is not necessary to maintain connectivity of the endochondral shoulder girdle to the skull. Our data support the possibility that the contribution of the neural crest to the endochondral shoulder girdle, which is observed in the mouse, arose de novo in mammals as a developmental basis for their skeletal synapomorphies. This further supports the hypothesis of an increased neural crest diversification during vertebrate evolution.

Defining the Axolotl Hematopoietic Stem Cell

Abstract 1295Hematopoietic stem cells (HSCs) are the most therapeutically usable stem cells to date. HSC derived cells are involved in wound healing responses throughout the body. The goal of our study is to discovery methods to promote improved regenerative responses from mammalian HSC. The champion of vertebrate regeneration is the axolotl. It can regrow entire limbs, major portions of most internal organs – including the brain and spinal cord. Recent advances in the production of transgenic axolotl, complete mapping of the axolotl transcriptome and production of gene expression arrays finally allow molecular mapping of regeneration pathways. In order to define the role of HSC in regeneration it was first necessary to define and characterize the axolotl HSC. In the current study we develop classic assays such as hematopoietic cell transplantations (HCT) and colony forming cell (CFC) assays to map axolotl hematopoiesis. In addition we take advantage of embryo manipulations possible with the axolotl to generate hematopoietic chimeras (GFP+ vs. white) as non-injury models for regeneration.Axolotl have a naturally occurring white variant that are nearly as transparent as zebrafish. We used a normal and CMV:GFP+ transgenic white strains to map sites of hematopoiesis and to develop HSC transplant methodology. We also establish protocols for Colony Forming Unit (CFU) assays for hematopoietic progenitors. Liver, spleen, kidney, marrow, and thymus were tested as potential HSC sources. Both the liver and spleen contained transplantable HSC capable of radioprotection and multilineage reconstitution of lethally irradiated (1000 rads) adult axolotls or non-conditioned embryos. As in zebrafish, use of the white axolotl mutant allows direct visualization of engraftment, homing, and hematopoiesis in real time. Fluorescent donor cells were seen homing to the liver and spleen regardless of tissue origin, albeit with better overall engraftment from spleen cells. Hematopoiesis occurred for more than 6 months in embryo transplantations. FACS analysis of these two organs showed that the liver contains relatively even numbers of myeloid and lymphoid populations whereas the spleen has a bias toward lymphoid and erythroid populations. Additionally, early stage white and GFP embryos were transected and the posterior and anterior halves of the two different animals were joined. GFP+ blood was present in animals that contained the liver or spleen within the GFP portion of the body further indicating that hematopoiesis occurs in these organs. These embryo chimeras also provide stable long-term GFP+ blood chimeras without irradiation injury. CFU assays demonstrated that the liver contains predominantly myeloid progenitors. In contrast, the spleen has mostly erythroid and megakaryocytic progenitors but also some myeloid progenitors.Here we have shown that the axolotl HSC resides in the liver and spleen and begun the basic mapping of hematopoiesis. Moreover, we have established the essential hematopoietic assays for the axolotl. The ability to generate both irradiation and non-injury GFP+ blood chimeras provide powerful tools to determine the role of HSC/progeny in axolotl regeneration. Disclosures:No relevant conflicts of interest to declare.

Neural crest cell migration and pigment pattern formation in urodele amphibians.

This review deals with research on the development and differentiation of the neural crest (NC) in amphibians carried out during the past twenty years. First, earlier studies on the migration and differentiation of NC cells in vitro are summarized. These studies include the modes of NC cell migration and their differentiation into chondroblasts, perichondral cells, neurons, Schwann cells and pigment cells (melanophores and xanthophores). Then a summary is given on the development of cranial sensory ganglia and enteric ganglia in Xenopus laevis. In the subsequent sections, mechanisms of NC cell migration are investigated in Ambystoma mexicanum, the Mexican axolotl (wild-type and white mutant) using ultrastructural, immunohistochemical and biochemical methods. In wild-type or dark axolotl embryos, pigment cells leave the NC and migrate out under the epidermis, whereas in the white mutant, pigment cells remain closely confined to the original position of the NC. This system provides an excellent model for analyzing NC cell migration in vertebrate embryos. Further sections deal with the development of larval pigment patterns in Triturus alpestris, (horizontal melanophore stripes) and Ambystoma mexicanum (vertical melanophore bars). Comparing the formation of these patterns shows that two different principles exist in the distribution of pigment derivatives of the NC: patterns following environmental cues (Triturus) and those ignoring these cues, relying solely on cell-cell interactions (Ambystoma). Other studies relate to evolutionary perspectives in pigment pattern formation. They are based on phylogenetic analyses of North American ambystomatids, combined with data on pigment patterns and their formation where such data are available. These studies have shown that vertical bars which develop from aggregates in the NC string are an evolutionary innovation, compared to the more primitive horizontal stripes lacking aggregates in the NC. Thus, in this review we show that the NC of amphibians (T. alpestris, Xenopus laevis, dark and white axolotls and other ambystomatids) may be used for various analyses concerning the migration and differentiation of its derivatives, as well as for studies on the formation and evolution of pigment patterns.

Effects of Melanocyte-Stimulating Hormone on Wild-Type and White Axolotl Neural Crest Cells

The goals of the current research were twofold: to study the effects of melanocyte-stimulating hormone (MSH) on undifferentiated axolotl ( Ambystoma mexicanum ) neural crest cells and to determine whether wild-type or white mutant axolotl neural crest cells respond differently to MSH or to either of two agonists of the MSH signal transduction pathway (cholera toxin or N 6,O 2-dibutyryl adenosine 3′,5′-monophosphate (dbcAMP). We found that MSH induces melanophore differentiation in axolotl neural crest cells in a dose-dependent manner; however, white, but not wild-type, neural crest cells are inhibited by the highest concentration of MSH (6 × 10 −6 M) tested. The effects of cholera toxin and dbcAMP indicate that the differentiation of melanophores from white neural crest cells may be more cAMP sensitive than wild-type neural crest cells. These results suggest that MSH is likely to play a regulatory role in the initial pigment pattern formation of wild-type and white axolotls.

Confrontation of Developing Melanophore Bars of Dark and White Axolotls With Endogenous Dark‐Embryo Mannose‐Binding Lectin Correlates With Melanophore Bar Disruption

Lectins are carbohydrate-binding proteins suggested to be important in embryonic cell adhesion/differentiation. Dark and white axolotls contain an endogenous mannose-binding lectin that is especially prevalent during larval melanophore pattern formation (Martha et al., 1990). To determine if this lectin can alter melanophore patterning, lectin extracts have been isolated from Dark embryos by affinity chromatography. The main protein band is 44K on SDS-PAGE. Dark and white embryos at the early chromatophore migration stage have been confronted with Dark lectin or its nonmetabolized inhibitor, 2-deoxyglucose (2-DG). The barred melanophore pattern of both genotypes is disrupted by lectin or 2-DG treatment suggesting that endogenous mannose-binding lectin and its receptor participate in bar formation.

Inhibition of neural crest cell differentiation by embryo ectodermal extract.

The white mutation in Mexican axolotls has long been thought to be a defect associated with the embryonic extracellular environment, but not with embryonic neural crest cells. Thus it was believed that pigment cells in white axolotls disappear from the skin during early development, not because they are intrinsically defective but because they have no choice but to move into an unfavorable environment. We present evidence to suggest that: (1) white neural crest cells are in fact intrinsically different from dark (wild-type) cells, and (2) an inhibitor is produced in white embryonic ectoderm that actively suppresses the migration, differentiation, and survival of pigment cells in this animal. How these observations fit into the existing body of literature on the white mutant and a model for how the white phenotype might develop are discussed.

Effects of fetal bovine serum and serum-free conditions on white and dark axolotl neural crest explants

Neural crest cells from both white mutant and dark (wildtype) axolotls (Ambystoma mexicanum) were cultured in increasing concentrations of fetal bovine serum (FBS; 2 to 20%). For each explant, the total number of cells that migrated and the percent of differentiated melanophores were recorded. At concentrations of FBS above 2% melanophore differentiation was essentially equivalent (32 to 59%) for both the white and dark neural crest cultures, but subtle differences in cell behavior and differentiation were found between the two phenotypes. By contrast there was a significant difference in the percent melanization of cells in serum-free control cultures, wherein melanophore differentiation in dark neural crest cultures was, on average, 18% compared to 5% in white cultures. Thus, contrary to all previously published work, white and dark neural crest cells are not intrinsically equivalent. Our culture results are discussed with regard to the probable in vivo conditions that cause the white phenotype.

Structural and compositional divergencies in the extracellular matrix encountered by neural crest cells in the white mutant axolotl embryo

The skin of the white mutant axolotl larva is pigmented differently from that of the normal dark due to a local inability of the extracellular matrix (ECM) to support subepidermal migration of neural crest-derived pigment cell precursors. In the present study, we have compared the ECM of neural crest migratory pathways of normal dark and white mutant embryos ultrastructurally, immunohistochemically and biochemically to disclose differences in their structure/composition that could be responsible for the restriction of subepidermal neural crest cell migration in the white mutant axolotl. When examined by electron microscopy, in conjunction with computerized image analysis, the structural assembly of interstitial and basement membrane ECMs of the two embryos was found to be largely comparable. At stages of initial neural crest cell migration, however, fixation of the subepidermal ECM in situ with either Karnovsky-ruthenium red or with periodate-lysine-paraformaldehyde followed by ruthenium red-containing fixatives, revealed that fibrils of the dark matrix were significantly more abundant in associated electron-dense granules. This ultrastructural discrepancy of the white axolotl ECM was specific for the subepidermal region and suggested an abnormal proteoglycan distribution. Dark and white matrices of the medioventral migratory route of neural crest cells had a comparable appearance but differed from the corresponding subepidermal ECMs. Immunohistochemistry revealed only minor differences in the distribution of fibronectin, laminin, collagen types I, and IV, whereas collagen type III appeared differentially distributed in the two embryos. Chondroitin- and chondroitin-6-sulfate-rich proteoglycans were more prevalent in the white mutant embryo than in the dark, especially in the subepidermal space. Membrane microcarriers were utilized to explant site-specifically native ECM for biochemical analysis. Two-dimensional gel electrophoresis of these regional matrices revealed a number of differences in their protein content, principally in constituents of apparent molecular masses of 30-90,000. Taken together our observations suggest that local divergences in the concentration/assembly of low and high molecular mass proteins and proteoglycans of the ECM encountered by the moving neural crest cells account for their disparate migratory behavior in the white mutant axolotl.

Developmentally regulated lectin in dark versus white axolotl embryos

The white mutant of the Mexican axolotl, A. mexicanum, involves an ectodermal defect which prevents melanophore colonization. Endogenous lectins have been suggested to function in neural crest-derived melanophore adhesion in other animals. To determine if differences in endogenous lectins exist in dark and white axolotls during melanophore colonization, white and dark ectoderm and carcass tissues have been assayed for lectin activity at premigratory, early migratory, and late migratory neural crest stages. Lectin content (specific for D-glucosamine, N-acetyl-D-glucosamine and D-mannose) increases significantly during early migration only in dark ectoderm and white carcass tissues, whereas white ectoderm and dark carcass lectin activities remain close to premigration levels. Neural crest cells in these embryos are associated with regions of high lectin activity suggesting that the differences in endogenous lectins may be involved in establishment of the dark/white phenotype.

Timing in the regulation of neural crest cell migration: Retarded “maturation” of regional extracellular matrix inhibits pigment cell migration in embryos of the white axolotl mutant

In larvae of the white axolotl mutant (Ambystoma mexicanum), contrary to normal dark ones, trunk pigmentation is restricted because the epidermis is unable to support subepidermal migration of pigment cells from the neural crest (NC). This study examines whether the subepidermal extracellular matrix (ECM) is the defective component which prevents pigment cell migration in the white embryo. We transplanted subepidermal ECM, adsorbed in vivo on membrane microcarriers, from and to white and dark embryos in various combinations. White embryos have demonstrated normal NC cell migration along the medioventral pathway, and in order to test the effects of medial ECM on subepidermal migration, this ECM was similarly transplanted. Carriers with ECM attached were inserted subepidermally in host embryos at a premigratory NC stage. Control carriers without ECM and carriers with subepidermal ECM from white donors did not affect NC cell migration in white or dark embryos. In contrast, subepidermal ECM from dark donors triggered NC cell migration in the subepidermal space of both white and dark hosts. Remarkably, subepidermal ECM from white donors which were older than those normally used also stimulated migration in embryos of both strains. Likewise, medial ECM from white donors elicited migration in white as well as dark hosts. Pigment cells occurred among those NC cells that were stimulated to migrate in response to contact with ECM on carriers. These results indicate that the subepidermal ECM of the white embryo is transiently defective as a substrate for pigment cell migration, implying that "maturation" of the ECM is retarded beyond the times during which pigment cells are able to respond. In contrast, the medial ECM of the white embryo appears to mature normally. These findings suggest that the effect of the d gene is expressed regionally through the subepidermal ECM during a limited period of development. Hence, the action of the d gene seems to retard ECM maturation, bringing it out of phase with the migratory capability of the pigment cells. We propose that such a shift in relative timing of the developmental phenomena involved inhibits pigment cell migration in embryos of the white axolotl mutant and, accordingly, that the restricted pigmentation of the mutant larva is generated through heterochrony.

Importance of timing in development: Retarded “maturation” of extracellular matrix inhibits pigment cell migration in embryos of the white axolotl mutant: [formula omitted]∗. Dept. of Zoology, Uppsala University, S-751 22 Uppsala, Sweden; ∗Dept. of Anatomy, Freiburg University, 7800 Freiburg, FRG

Importance of timing in development: Retarded “maturation” of extracellular matrix inhibits pigment cell migration in embryos of the white axolotl mutant: [formula omitted]∗. Dept. of Zoology, Uppsala University, S-751 22 Uppsala, Sweden; ∗Dept. of Anatomy, Freiburg University, 7800 Freiburg, FRG

Neural crest cell behavior in white and dark larvae of Ambystoma mexicanum: differences in cell morphology, arrangement, and extracellular matrix as related to migration.

Melanocytes of white (d/d) larvae of the Mexican axolotl (Ambystoma mexicanum) are confined to the dorsal midline of the trunk region, whereas in dark (D/-) larvae they are spread laterally on the flank as well, where they contribute to the normal pigment pattern of the trunk. Pigment cell migration in the subepidermal space of white larvae is inhibited by the white epidermis (Dalton '50; Keller et al., '82). The present scanning electron microscopic study describes a well-defined sequence of changes in shape and arrangement of neural crest cells during and after their segregation from the neural tube in both dark and white axolotls. The morphology of the neural crest cells migrating in the subepidermal pathway of dark larvae is correlated with their motile behavior and pattern of migration in vivo, as described by time-lapse cinemicrography (Keller and Spieth, '83). Also, the structures of the matrix material in the subepidermal space of dark and white axolotls differ in ways that may be related to the epidermal inhibition of migration in the latter. Numerous possibilities for contact guidance offered by the structure and topography of the substrata, neighboring cells, and the extracellular matrix in the migration path are described and discussed.

Neural crest cell behavior in white and dark embryos of Ambystoma mexicanum: Epidermal inhibition of pigment cell migration in the white axolotl

Melanophores in larvae of the white ( dd) strain of the Mexican axolotl ( Ambystoma mexicanum) are confined to the dorsal midline of the trunk and dorsal posterior part of the head, whereas those in dark larvae ( D -) are distributed over the flank as well. Our results show that this phenotype of white larvae is the result of the failure of the melanophores or their neural crest precursor cells to migrate laterally due to an inhibition of or a failure in the support of their migration in the subepidermal space by the overlying epidermis. Correlated light and scanning electron microscopy of dissected larvae showed melanophores occupying the subepidermal space on the flank of dark larvae, whereas these cells were restricted to the dorsal midline of white larvae. Grafting experiments in which patches of epidermis, the underlying mesoderm, or both, were exchanged between dark and white embryos suggested that white epidermis alone can prevent the integration of pigment cells on the flank of dark larvae and, conversely, that grafts of dark epidermis alone can support their migration on the flank of white larvae. Mesoderm, when grafted alone, could not be shown to have similar effects.

Gene action on proliferation and migration in the developing neural crest of black and white axolotls, Ambystoma mexicanum, Shaw.

AbstractThe mitotic index \documentclass{article}\pagestyle{empty}\begin{document}$ \left({\frac{{{\rm number\,of\,dividing\,cells}}}{{{\rm total\,number\,of\,cells}}}} \right) $\end{document} of the neural crest and its derivatives in situ was determined in serially‐sectioned embryos of the black (DD or Dd) and white (dd) strains of the Mexican axolotl, Ambystoma mexicanum, Shaw, to see whether the differences between the strains in the number and distribution of their initial complement of melanophores could be causally related to differences in the pattern of development of their respective neural crests.Prior to and during the initial appearance of melanophores, the mitotic index of the neural crest in situ in the black axolotl is significantly greater than in the white. Concommitantly, there are more crest cells in the black than in the white prior to crest cell migration. However, during the periods of maximum crest cell migration and initial appearance of melanophores, there are significantly more crest cells in situ in the white than in the black. These crest cells in situ in the white are clumped together mid‐dorsal to the neural tube, while in the black they show the dispersion typical of migrating crest cells.Following the initial appearance of melanophores, there are no differences between the strains in the number of melanophores dorsal to the neural tube and somites, but there are significantly more crest‐derived cells in this area in the black than in the white. The latter difference between the strains may be causally related to the significantly greater number of cells in the early spinal ganglia of the black axolotl than in the white.

Developmental potentialities of blastema cell nuclei of the Mexican Axolotl.

AbstractDuring amphibian limb regeneration, differentiated cells contribute to the formation of a blastema. Cells once incorporated into the blastema are identical in their morphological appearances. This investigation is a test of the developmental potentialities of blastema cell nuclei as revealed by means of nuclear transplantation.When blastula cell nuclei are injected into enucleated eggs, approximately 80–90% of the test eggs cleave. Over half of the cleaved eggs form regular blastulae. Of the regular blastuae 60% form post‐neurula embryos.The initial experiment with regenerating cells involved the ijection of two to three blastema cell nuclei from a seven‐day‐old regenerate into test eggs. The blastema cells were obtained from a white Axolotl (dd) and the test eggs were laid by a dark Axolotl (Dd). Of some 35 eggs injected, five partial and two regular blastulae were obtained. One of the regular blastulae was sacrificed after 24 hours of development, and part of its tissue was grafted on an embryo of the genetic composition DD. When the host started to develop its pigmentation, the graft developed as a white patch, thus indicating the genetic nature of the graft was that of transplanted blastema cell nucleus. Subsequently single blastema cell nuclei from seven‐ to sixteen‐day‐old regenerates were injected into test eggs. Blastema cell nuclei of eight‐day‐old regenerates were injected into test eggs. Blastema cell nuclei of eight‐day‐old regenerates were able to promote development of post neurula embryos.

The biochemical effects of the d, m, and a genes on pigment cell differentiation in the axolotl

Summary Three mutations alter the basic pigmentation of the wild-type axolotl. In this study an attempt has been made to describe the biochemical alterations associated with these mutations and to correlate them with the cellular changes observed by other investigators and verified by this author. The a gene has no effect on either pteridine or purine synthesis or on xanthophore or iridiophore differentiation. Rather, it inactivates tyrosinase completely, resulting in the absence of melanin in albino axolotls. The effects of the m gene are primarily on the production of propigment cells by the neural crest. Transplants indicate that more melanophores and fewer xanthophores (than in the wild-type), and no iridiophores are produced in axolotls homozygous for m. Correlated with these observations are a 35% increase in tyrosinase activity and a 40% decrease in pteridine synthesis in melanoid animals. The former may, in part, be due to an increased amount of tyrosinase in each melanophore. Moreover, an accumulation of IDP + ITP, AMP, and an unidentified purine derivative suggest that a somewhat “leaky” enzymatic block in the conversion of IMP into XMP (or of XMP into GMP) may contribute to the reduction and absence, respectively, of fully differentiated xanthophores and iridiophores in melanoid skin. The extent of these contributions remains to be determined. Transplantation experiments indicate that the d gene does not alter the production of propigment cells by the neural crest. The 70% decrease in melanin synthesis (and melanophores) in white axolotls appears to be the result of decreased tyrosinase activity rather than of inhibited melanoblast migration. Likewise, the 50% decrease in pteridine synthesis (and xanthophores) appears to be the result of both decreased (40%) glucose-6-phosphate dehydrogenase activity during embryonic stages and of a “leaky” enzymatic block in the conversion of GMP into biopterin, rather than a result of inhibited xanthoblast migration. Since the former block is operative only during embryonic stages, and since the latter block results in a shunting of GMP into guanine synthesis, normal iridiophore differentiation occurs in axolotls homozygous for d.

Genetic and experimental studies on a lethal trait (“Short Toes”) in the Mexican axolotl (Ambystoma mexicanum)

AbstractA recessive lethal factor (s) discovered in the Mexican axolotl induces (1) reduction in length of limbs and number of phalanges, (2) failure of complete development of Mullerian ducts, and (3) renal pathology and dysfunction leading to death.Larvae homozygous for s, in parabiosis with normal animals, show no improvement in length of limbs or number of phalanges. Transplants of the forelimb area between normal and s/s embryos produce limbs of donor type. The character of the limbs in the s/s thus appears independent of nutritional or hormonal influences.The Mullerian ducts of s/s reared as parabionts with normal animals remain incomplete. The duct derived from a pronephric transplant from an s/s into a normal embryo attains full length, however, as does the duct from the reciprocal type of transplant. Probably intrinsic factors in duct epithelium and related stroma combine in s/s larvae to limit duct growth.Death of affected animals usually occurs before they are one year of age. Although some attain sexual maturity, none has reproduced.Gene s was probably carried by some of the white axolotls imported from Cracow by the Wistar Institute in the early 1930's. No linkage with other genes has been demonstrated.

Pigment cell development after exchange of neural folds between the california newt and the mexican axolotl

AbstractTrunk neural folds from both black and white axolotls, Ambystoma mexicanum, were transplanted unilaterally in place of folds of Taricha torosa neurulae. Melanophores from either kind of axolotl completely suppress the differentiation of T. torosa melanophores for several stages and largely suppress it for much longer. During larval stages host pigmentation gradually develops, but axolotl pigmentation always dominates. After metamorphosis the typical Ambystoma spotted pattern appears. During all stages donor melanophores are almost equally distributed on both flanks, with only slightly more on the grafted side. Guanophores predominate on the grafted side, while xanthophores predominate on the opposite side. With the exception of the distribution of axolotl melanophores, these results confirm results of others with the black axolotl and offer additional evidence that the chromatophores of both black and white axolotls are equivalent. New suggestions are made to explain the unequal distribution of xanthophores and guanophores in view of the nearly equal distribution of axolotl melanophores.Trunk neural folds of T. torosa were transplanted bilaterally in place of white axolotl neural folds. The typical T. torosa larval pigment pattern is expressed in the grafted area, but host melanophores suppress donor melanophores beyond the confines of the graft. Eventually all axolotls immunologically rejected their neural crest grafts. Only 13% of the T. torosa rejected their grafts. These results confirm that T. torosa has a much greater tolerance to grafted foreign tissue than do axolotls. The immunological behavior of these animals is discussed in the context of results of similar experiments in anurans.

Pituitary influence on pigment pattern development in the white axolotl

Journal of Experimental ZoologyVolume 133, Issue 2 p. 241-257 Article Pituitary influence on pigment pattern development in the white axolotl† H. Clark Dalton, H. Clark Dalton Washington Square College of Arts and Science New York University New York 3, N. YSearch for more papers by this authorZonia P. Krassner, Zonia P. Krassner Washington Square College of Arts and Science New York University New York 3, N. YSearch for more papers by this author H. Clark Dalton, H. Clark Dalton Washington Square College of Arts and Science New York University New York 3, N. YSearch for more papers by this authorZonia P. Krassner, Zonia P. Krassner Washington Square College of Arts and Science New York University New York 3, N. YSearch for more papers by this author First published: November 1956 https://doi.org/10.1002/jez.1401330204Citations: 10 † These investigations were supported in part by a research grant from the Damon Runyan Memorial Fund. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume133, Issue2November 1956Pages 241-257 RelatedInformation