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PubMed1998

Modulation of the chaperone heat shock cognate 70 by embryonic (pro)insulin correlates with prevention of apoptosis.

Insights have emerged concerning insulin function during development, from the finding that apoptosis during chicken embryo neurulation is prevented by prepancreatic (pro)insulin. While characterizing the molecules involved in this survival effect of insulin, we found insulin-dependent regulation of the molecular chaperone heat shock cognate 70 kDa (Hsc70), whose cloning in chicken is reported here. This chaperone, generally considered constitutively expressed, showed regulation of its mRNA and protein levels in unstressed embryos during early development. More important, Hsc70 levels were found to depend on endogenous (pro)insulin, as shown by using antisense oligodeoxynucleotides against (pro)insulin mRNA in cultured neurulating embryos. Further, in the cultured embryos, apoptosis affected mainly cells with the lowest level of Hsc70, as shown by simultaneous Hsc70 immunostaining and terminal deoxynucleotidyltransferase-mediated UTP nick end labeling. These results argue in favor of Hsc70 involvement, modulated by embryonic (pro)insulin, in the prevention of apoptosis during early development and suggest a role for a molecular chaperone in normal embryogenesis.

Amino Acid Sequence↗

PubMed1998

Effect of thymosin fraction five (TF5) on early neuroembryogenesis in the newt Triturus cristatus.

Thymosin fraction five (TF5), a well-characterized immunoregulatory thymic preparation, has been reported to stimulate corticotropin (ACTH) release. The present study explores the morphogenetic role of TF5 on early stages of nerve tissue formation during embryogenesis. In vivo TF5-treatment of newt embryos during neurulation results in stimulation of the process expressed at a macro-microscopical level by emphasizing the embryo's relief and by accelerating the neural tube closure. The stimulating effect of TF5 on neurulation is manifested ultrastructurally by enhanced apical endocytosis, a well-developed contractile microfilamentous layer, increased apical intercellular junctions and changes of the cytoplasmic organelles linked with the protein synthesis. The polymorphism of mitochondria and the morphological expression of enhanced yolk material assimilation confirm the idea of TF5-stimulating effect on the neuroepithelial cells.

Animals↗

PubMed1998

Cloning of a complementary DNA encoding an Ambystoma mexicanum metallothionein, AmMT, and expression of the gene during early development.

We have used a polymerase chain reaction strategy to isolate a metallothionein (MT) cDNA from the amphibian Ambystoma mexicanum (axolotl). This cDNA is 875-bp long and encodes a 60 amino acid protein, AmMT, typical for family 1 MTs. It contains 20 cysteine (Cys) residues that can be aligned with those of other vertebrate MTs. The overall structure of the protein is unique among vertebrates in having only two amino acid residues before the first Cys at the amino-terminal end. Northern analyses showed that AmMT is expressed throughout embryogenesis, giving rise to three mRNA species of 650, 750, and 1,600 nucleotides (nt). The 750 and 1,600 nt transcripts appear to result from differential use of polyadenylation signals, whereas the 650 nt RNA could arise from deadenylation of the 750-nt transcript. Both the 750- and 1,600-nt RNAs were presented in embryos before the mid-blastula transition (MBT). After the MBT, the 750-nt RNA was replaced by the 650-nt RNA which was gradually degraded to undetectable levels in post-neurulation embryos. Levels of the 1,600-nt transcript increased at gastrulation and reach a maximum in Stage 30 embryos. In adult animals, levels of the 750-nt RNA were high in liver and testes, and very low in lung, gut, skin, and oviducts, whereas levels of the 1,600-nt transcript were similar and moderately elevated in all tissues examined. In contrast, in Xenopus laevis, Northern analysis did not detect XIMT-A mRNA in embryos before late neurulation (Stage 24). XIMT-A mRNA levels then increased sharply in Stage 36 hatched embryos at levels similar to those found in adult livers. These results show that AmMT presents a unique expression pattern among metazoans being transcribed as two transcripts differing in the length of their 3' untranslated regions, the levels of which vary during embryogenesis and in adult tissues.

Ambystoma↗

PubMed2001

Severe neural tube defects in the loop-tail mouse result from mutation of Lpp1, a novel gene involved in floor plate specification.

Neural tube defects (NTD) are clinically important congenital malformations whose molecular mechanisms are poorly understood. The loop-tail (Lp) mutant mouse provides a model for the most severe NTD, craniorachischisis, in which the brain and spinal cord remain open. During a positional cloning approach, we have identified a mutation in a novel gene, Lpp1, in the Lp mouse, providing a strong candidate for the genetic causation of craniorachischisis in LP: Lpp1 encodes a protein of 521 amino acids, with four transmembrane domains related to the Drosophila protein strabismus/van gogh (vang). The human orthologue, LPP1, shares 89% identity with the mouse gene at the nucleotide level and 99% identity at the amino acid level. Lpp1 is expressed in the ventral part of the developing neural tube, but is excluded from the floor plate where Sonic hedgehog (Shh) is expressed. Embryos lacking Shh express Lpp1 throughout the ventral neural tube, suggesting negative regulation of Lpp1 by SHH: Our findings suggest that the mutual interaction between Lpp1 and Shh may define the lateral boundary of floor plate differentiation. Loss of Lpp1 function disrupts neurulation by permitting more extensive floor plate induction by Shh, thereby inhibiting midline bending of the neural plate during initiation of neurulation.

Amino Acid Sequence↗

PubMed2003

Specific isoforms of protein kinase C are essential for prevention of folate-resistant neural tube defects by inositol.

A proportion of neural tube defects (NTDs) can be prevented by maternal folic acid supplementation, although some cases are unresponsive. The curly tail mutant mouse provides a model of folate-resistant NTDs, in which defects can be prevented by inositol therapy in early pregnancy. Hence, inositol represents a possible novel adjunct therapy to prevent human NTDs. The present study investigated the molecular mechanism by which inositol prevents mouse NTDs. Activation of protein kinase C (PKC) is known to be essential, and we examined neurulation-stage embryos for PKC expression and applied PKC inhibitors to curly tail embryos developing in culture. Although all known PKC isoforms were detected in the closing neural tube, use of chemical PKC inhibitors identified a particular requirement for 'conventional' PKC isoforms. Peptide inhibitors offer selective inhibition of individual PKCs, and we demonstrated isoform-specific inhibition of PKC in embryonic cell cultures. Application of peptide inhibitors to neurulation-stage embryos revealed an absolute dependence on the activity of PKCbetaI and gamma for prevention of NTDs by inositol, and partial dependence on PKCzeta, whereas other PKCs (alpha, betaII delta, and epsilon) were dispensable. To investigate the cellular action of inositol and PKCs in NTD prevention, we examined cell proliferation in curly tail embryos. Defective proliferation of hindgut cells is a key component of the pathogenic sequence leading to NTDs in curly tail. Hindgut cell proliferation was stimulated specifically by inositol, an effect that required activation of PKCbetaI. Our findings reveal an essential role of specific PKC isoforms in mediating the prevention of mouse NTDs by inositol.

Animals↗

PubMed1983

Neural tube defects: clinical correlations.

There are several approaches that can be applied to the analysis of malformations of the CNS. One practical way in making clinical correlations is to divide neural tube defects into those that arise during the period of neurulation and those that arise thereafter. This concept applies to cranial and spinal lesions and makes it possible to interpret clinical findings with embryological events. Malformations of the CNS that arise during the period of neurulation are not covered by skin and can be diagnosed prenatally by amniocentesis. Postneurulation CNS malformations are skin-covered and have differing patterns of associated malformation and etiologies. There is an overlap of the latter group with congenital tumors, and for the most part these malformations are not apt to be diagnosed prenatally.

Anencephaly↗

PubMed2002

Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro.

A role for choline during early stages of mammalian embryogenesis has not been established, although recent studies show that inhibitors of choline uptake and metabolism, 2-dimethylaminoethanol (DMAE), and 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3), produce neural tube defects in mouse embryos grown in vitro. To determine potential mechanisms responsible for these abnormalities, choline metabolism in the presence or absence of these inhibitors was evaluated in cultured, neurulating mouse embryos by using chromatographic techniques. Results showed that 90%-95% of 14C-choline was incorporated into phosphocholine and phosphatidylcholine (PtdCho), which was metabolized to sphingomyelin. Choline was oxidized to betaine, and betaine homocysteine methyltransferase was expressed. Acetylcholine was synthesized in yolk sacs, but 70 kDa choline acetyltransferase was undetectable by immunoblot. DMAE reduced embryonic choline uptake and inhibited phosphocholine, PtdCho, phosphatidylethanolamine (PtdEtn), and sphingomyelin synthesis. ET-18-OCH3 also inhibited PtdCho synthesis. In embryos and yolk sacs incubated with 3H-ethanolamine, 95% of recovered label was PtdEtn, but PtdEtn was not converted to PtdCho, which suggested that phosphatidylethanolamine methyltransferase (PeMT) activity was absent. In ET-18-OCH3 treated yolk sacs, PtdEtn was increased, but PtdCho was still not generated through PeMT. Results suggest that endogenous PtdCho synthesis is important during neurulation and that perturbed choline metabolism contributes to neural tube defects produced by DMAE and ET-18-OCH3.

Acetylcholine↗

PubMed1991

A retinoic acid receptor expressed in the early development of Xenopus laevis.

We have isolated cDNAs coding for a putative retinoic acid receptor (RAR) of the gamma-type from a Xenopus laevis neurula cDNA library. By transient cotransfection of COS cells with an expression vector and a reporter plasmid, this cDNA is shown to direct the synthesis of a retinoic acid-dependent transcription factor. In embryos of X. laevis, transcription of the corresponding gene is greatly enhanced during gastrulation and early neurulation. Two distinct areas with high abundance of RAR gamma mRNA are located at the anterior and at the posterior end of the neurula. The two maxima have emerged by the end of gastrulation and they become more pronounced during neurulation. At tailbud and early tadpole stages, the RAR transcripts are found mainly in the head mesenchyme and in the tailbud. The expression of this RAR is region-specific but not germ-layer-specific. The strong and stage-specific activation of zygotic transcription of this RAR gene, and the specific localization of the mRNA are consistent with the temporal and spatial pattern of retinoic acid sensitivity of X. laevis embryos. Therefore it is likely that the gene product mediates the effects of endogenous and of exogenous retinoic acid on early embryogenesis of Xenopus. The significance of these findings for the specification of the anteroposterior axis is discussed.

Amino Acid Sequence↗

PubMed1993

Molecular analysis of the Wnt-1 proto-oncogene in Ambystoma mexicanum (axolotl) embryos.

To analyze Wnt-1 expression during neurulation in urodele embryos, we have isolated a Wnt-1 cDNA clone, Awnt-1, from an Ambystoma mexicanum (axolotl) neurula-stage cDNA library. Awnt-1 codes for a protein of 369 amino acids rich in cysteine residues, is preceded by a hydrophobic leader peptide sequence and contains four possible sites for N-linked glycosylation. The temporal expression profile of Awnt-1 was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Awnt-1 expression in the axolotl embryo is biphasic. Awnt-1 transcripts are found in early blastulae until gastrulation, are barely detectable during gastrulation, and are present again from neurulation until late embryogenesis. Transcripts are present before the midblastula transition, indicating that they might be of maternal origin. To localize Awnt-1 expression in embryos during the first phase of expression, early gastrulae were dissected by cutting along the animal-vegetal and future dorso-ventral axes and analyzed by RT-PCR. At the early gastrula stage Awnt-1 transcripts appear to be located in the future ventral region of the embryo. Hatching larvae no longer express Awnt-1. PCR reactions performed using cDNA library-phage DNA templates derived from whole neurulae versus embryos with the neuroectoderm removed suggest that, in the neurula, Awnt-1 transcripts are located in the neuroectoderm. This suggest that, as is the case for Wnt-1 in other vertebrates, Awnt-1 may be involved in neurogenesis. These results suggest that Wnt-1 has earlier roles in development than has been considered until now.

Ambystoma mexicanum↗

PubMed1983

The distribution of small ions during the early development of Xenopus laevis and Ambystoma mexicanum embryos.

The free ion concentrations of Na+, K+ and Cl- have been measured in the cells and intercellular spaces of developing amphibian embryos using ion-sensitive microelectrodes. Ca2+, H+ and buffering capacity have also been measured in the intercellular spaces. The free intracellular Na+ and K+ concentrations in the early cleavage stages remain approximately constant at 21 mM and 90 mM respectively. The free intracellular Cl- concentration, approximately 60 mM during the egg to 4-cell stage, falls during development to around 30 mM by the 128-cell stage. Embryos from different batches show a wide variation in intracellular free ion content. A strong correlation was observed between the ion content, particularly of K+, and the viability of the embryo. If the intracellular K+ concentration was less than 60 mM, embryos invariably died between late blastula and early gastrula stages; if greater than 80 mM the embryo generally survived. The intercellular free Na+, K+, Cl- and Ca2+ concentrations in Xenopus mid-blastula embryos are 91 mM, 4 mM, 59 mM and 1.5 mM respectively. The intercellular potential at late neurula stages is +3.5 mV when the embryo is bathed in 5% Ringer solution; changing to Ringer solution reduced the potential to -4 mV. Before gastrulation the intercellular Ca2+ concentration in Xenopus falls to approximately 0.5 mM, where it remains throughout gastrulation before returning to its mid-blastula value during neurulation. In Xenopus, the intercellular Na+ concentration falls to around 75 mM and the intercellular K+ concentration rises to around 17 mM at the end of gastrulation. These changes are not maintained and both Na+ and K+ concentrations return to their earlier values. In Ambystoma, the intercellular K+ concentration falls steadily from 7 mM at the mid-blastula stage to 2 mM at the end of neurulation. The Na+ concentration is constant at approximately 93 mM up to stage 14; between stages 14 and 16 the measurements show some scatter (minimum value 60 mM, maximum value 100 mM), and beyond stage 16 the Na+ concentration increases to 123 mM.

Ambystoma↗

PubMed2004

The primitive streak, the caudal eminence and related structures in staged human embryos.

The caudal region of the trunk was reassessed in 52 serially sectioned human embryos of stages 8-23, 42 of which were controlled by precise graphic reconstructions. The following observations, new for the human, are presented. (1) The neurenteric canal is an important landmark because rostral to it the neural plate of stages 8, 9, and the main part of the notochord develop, whereas caudal to it the neural plate of stages 10-12 and the caudal portion of the notochord are formed. All somites at stages 9-11 and probably also at stage 12 arise rostral to the site of the neurenteric canal. (2) A 'chordoneural hinge' can be detected in stages 10 and 11, where the caudal part of the neural plate gives off cells that probably participate in the production of mesenchyme. (3) When apparent disappearance of the epiblast is used as a criterion, then the primitive streak seems to end during stage 9. (4) The caudal eminence, derived from the primitive streak and covered by ectoderm, forms at stage 10 caudal to the site of the former neurenteric canal and persists as a terminal cap to at least stage 14, although formation of mesenchyme continues in stages 15 to 17 or 18. (5) As the region rostral to the site of the neurenteric canal grows because of the development of somites, the caudal eminence is shifted caudally. (6) The caudal eminence is most active developmentally during stage 13, when most of the required (ca 6 out of 9) pairs of somites appear. (7) The eminence produces the caudal part of the notochord and, after closure of the caudal neuropore, all caudal structures, but it does not produce even a temporary 'tail' in the human. (8) A temporal overlap results between primary and secondary development in the caudal part of the notochord. (9) Primary development begins very early with the formation of the inner cell mass at stage 3, and includes the development of the somites rostral to the neurenteric canal, whereas secondary development, with the exception of the notochord caudally, commences at stage 12. (10) Primary neurulation lasts from stage 8 to stage 12, secondary from stage 12 to stages 17 or 18. (11) Secondary development and secondary neurulation are characterized morphologically by direct formation of structures (notochord, postcloacal gut, neural cord/neural tube) from mesenchyme.

Ectoderm↗

PubMed1995

Mechanisms of mutant genes in spina bifida: a review of implications from animal models.

Spina bifida (spinal neural tube defects) has been shown to be caused by an abnormality in closure of the neural tube. Basic scientific research has rapidly progressed in experimental embryology and molecular genetics to give new insights into the pathogenesis of defective neural tube closure. The chick and the mouse have proved to be the best animal models for study because of similarities to human neurulation. The embryonic mechanisms for spina bifida appear to be under the control of mutant early regulating genes and modifying genes. Faulty early gene function in chicks and mice has been reported to result in abnormalities of neuronal and nonneuronal tissues important for neural tube closure. Research efforts are being aimed at understanding the inductive interactions and downstream target sites for early regulating genes. Elucidation of the genetic roadmap for the control of neurulation will give further insights into the causes of spina bifida.

Animals↗

PubMed1997

Role of prepancreatic (pro)insulin and the insulin receptor in prevention of embryonic apoptosis.

The characterization of (pro)insulin as an early embryonic growth factor requires demonstration of its expression and cellular effects in vivo. By in situ hybridization, we found widespread preproinsulin transcripts in the chick embryo throughout gastrulation and neurulation, before the beginning of preproinsulin-like growth factor I expression and pancreatic organogenesis. To analyze the prepancreatic (pro)insulin effect on apoptotic cell death, we treated embryos with antisense oligodeoxynucleotides in ovo and in vitro. The specific effect of two preproinsulin messenger RNA (mRNA) antisense oligodeoxynucleotides was confirmed by the decrease in a biosynthetically labeled protein immunoprecipitated with antiinsulin Igs. Insulin receptor mRNA antisense oligodeoxynucleotide applied in ovo increased by 2.7-fold the level of apoptosis in the 1.5-day embryo (neurulation) compared with that in its random sequence control. In a whole embryo culture, apoptosis increased by 25-35% with the addition of preproinsulin or insulin receptor mRNAs antisense oligodeoxynucleotides, respectively, whereas it decreased by 64% after 10 h in the presence of 10(-8) M chicken insulin. Exogenous insulin also rescued the death induced by preproinsulin antisense oligonucleotides. These findings provide evidence for an autocrine/paracrine role ofpreproinsulin gene products acting through the insulin receptor in the control of cell survival/death during early embryonic development.

Animals↗

PubMed2007

Convergent extension, planar-cell-polarity signalling and initiation of mouse neural tube closure.

Planar-cell-polarity (PCP) signalling is necessary for initiation of neural tube closure in higher vertebrates. In mice with PCP gene mutations, a broad embryonic midline prevents the onset of neurulation through wide spacing of the neural folds. In order to evaluate the role of convergent extension in this defect, we vitally labelled the midline of loop-tail (Lp) embryos mutant for the PCP gene Vangl2. Injection of DiI into the node, and electroporation of a GFP expression vector into the midline neural plate, revealed defective convergent extension in both axial mesoderm and neuroepithelium, before the onset of neurulation. Chimeras containing both wild-type and Lp-mutant cells exhibited mainly wild-type cells in the midline neural plate and notochordal plate, consistent with a cell-autonomous disturbance of convergent extension. Inhibitor studies in whole-embryo culture demonstrated a requirement for signalling via RhoA-Rho kinase, but not jun N-terminal kinase, in convergent extension and the onset of neural tube closure. These findings identify a cell-autonomous defect of convergent extension, requiring PCP signalling via RhoA-Rho kinase, during the development of severe neural tube defects in the mouse.

Animals↗

PubMed2003

Glypican 4 modulates FGF signalling and regulates dorsoventral forebrain patterning in Xenopus embryos.

Heparan sulphate proteoglycans such as glypicans are essential modulators of intercellular communication during embryogenesis. In Xenopus laevis embryos, the temporal and spatial distribution of Glypican 4 (Gpc4) transcripts during gastrulation and neurulation suggests functions in early development of the central nervous system. We have functionally analysed the role of Xenopus Gpc4 by using antisense morpholino oligonucleotides and show that Gpc4 is part of the signalling network that patterns the forebrain. Depletion of GPC4 protein results in a pleiotropic phenotype affecting both primary axis formation and early patterning of the anterior central nervous system. Molecular analysis shows that posterior axis elongation during gastrulation is affected in GPC4-depleted embryos, whereas head and neural induction are apparently normal. During neurulation, loss of GPC4 disrupts expression of dorsal forebrain genes, such as Emx2, whereas genes marking the ventral forebrain and posterior central nervous system continue to be expressed. This loss of GPC4 activity also causes apoptosis of forebrain progenitors during neural tube closure. Biochemical studies establish that GPC4 binds FGF2 and modulates FGF signal transduction. Inhibition of FGF signal transduction, by adding the chemical SU5402 to embryos from neural plate stages onwards, phenocopies the loss of gene expression and apoptosis in the forebrain. We propose that GPC4 regulates dorsoventral forebrain patterning by positive modulation of FGF signalling.

Animals↗

PubMed2006

A dynamic fate map of the forebrain shows how vertebrate eyes form and explains two causes of cyclopia.

Mechanisms for shaping and folding sheets of cells during development are poorly understood. An example is the complex reorganisation of the forebrain neural plate during neurulation, which must fold a sheet into a tube while evaginating two eyes from a single contiguous domain within the neural plate. We, for the first time, track these cell rearrangements to show that forebrain morphogenesis differs significantly from prior hypotheses. We postulate a new model for forebrain neurulation and demonstrate how mutations affecting two signalling pathways can generate cyclopic phenotypes by disrupting normal cell movements or introducing new erroneous behaviours.

Animals↗

PubMed1987

Basal lamina is not a barrier to neural crest cell emigration: documentation by TEM and by immunofluorescent and immunogold labelling.

One of the factors proposed to control initiation of migration of neural crest (NC) cells is disruption of the basal lamina (BL) that is presumed to exist over the dorsal portion of the neural tube. Previously, we discovered that, in the mouse embryo, a continuous BL is not deposited over the dorsal portion of the neural tube until emigration of the NC cells is terminated. Here, we show that the pattern of BL deposition in chick embryos is similar, but not identical, to that in the mouse. In particular, (i) patches of BL are deposited on the premigratory NC cells in the chick but not in the mouse and (ii) BL is thicker and more interstitial matrix is deposited at the same stage of development in the chick. In addition, immunofluorescent and immunogold labelling of collagen IV, laminin and fibronectin show that (i) patches of young BL contain all three molecules; (ii) collagen IV and laminin are present in BL throughout neurulation but fibronectin either disappears or becomes masked in more mature BL and (iii) collagen IV and especially fibronectin are present in the interstitial matrix, but the relative abundance of fibronectin changes with time. The simultaneous use of immunolabelling for both light and TEM sections has allowed us to determine unambiguously that presence of a basement membrane (light microscopy) does not necessarily imply presence of basal lamina. We conclude that, as in mouse, the BL cannot be involved in the timing of the initiation of migration of NC cells. Our evidence in both the mouse and the chick, together with work in the axolotl, suggests that the basic pattern of BL deposition during neurulation may be a general phenomenon in embryonic development. Moreover, these results, in conjunction with the work of others, suggest that the critical step for initiation of migration of NC cells may be the loss of adhesions between cells.

Animals↗

PubMed1989

Roles of neuroepithelial cell rearrangement and division in shaping of the avian neural plate.

Shaping of the neural plate, one of the most striking events of neurulation, involves rapid craniocaudal extension. In this study, we evaluated the roles of two processes in neural plate extension: neuroepithelial cell rearrangement and cell division. Quail epiblast plugs of constant size were grafted either just rostral to Hensen's node or paranodally and the resulting chimeras were examined at selected times postgrafting. By comparing the size of the original plug, the number of cells it contained and the distribution of cells within it to those same features of the grafts in chimeras, we were able to ascertain that, during transformation of the flat neural plate into the closed neural tube (a period requiring 24 h), the graft undergoes a maximum of 3 rounds of craniocaudal extension (each round of craniocaudal extension was defined as a doubling of graft length, so 3 rounds equaled an 8-fold increase in length). Such extension is accompanied by 2 rounds of cell rearrangement and 2-3 rounds of cell division (cell rearrangement occurred mediolaterally, so each round was defined as a halving of the number of cells in the width of the graft and a doubling of the number of cells in its length; each round of cell division was defined as a doubling of graft cell number). Modeling studies demonstrate that these amounts of cell rearrangement and division are sufficient to approximate the shaping of the neural plate that normally ensues during neurulation, provided that some of the cell division occurs within the longitudinal plane of the neural plate and some within its transverse plane: longitudinal cell division results in craniocaudal extension of the neural plate, whereas transverse cell division results in lateral expansion of the neural plate such as that occurring at its cranial end; cell rearrangement results in craniocaudal extension of the neural plate as well as in its narrowing. In conclusion, our results provide evidence that shaping of the neural plate involves mediolateral cell rearrangement and cell division, with the latter occurring within both the longitudinal and transverse planes of the neural plate.

Animals↗