Talk:Frog Development - Revision history

Z8600021 at 07:08, 7 December 2021

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	==~~10 Most Recent Papers~~==		==2021==
	~~{{10 Most Recent}}~~

	~~===Frog Development===~~		Pinhead antagonizes Admp to promote notochord formation
	~~<pubmed limit=5>Frog Development</pubmed>~~

	~~===Frog Embryology===~~		Keiji Itoh 1 , Olga Ossipova 1 , Sergei Y Sokol 1
	~~<pubmed limit=5>Frog Embryology<~~/~~pubmed>~~		Affiliations expand
			PMID: 34142034 PMCID: PMC8188501 DOI: 10.1016/j.isci.2021.102520
			Free PMC article
			Abstract

			Dorsoventral patterning of a vertebrate embryo critically depends on the activity of Smad1 that mediates signaling by BMP proteins, anti-dorsalizing morphogenetic protein (Admp), and their antagonists. Pinhead (Pnhd), a cystine-knot-containing secreted protein, is expressed in the ventrolateral mesoderm during Xenopus gastrulation; however, its molecular targets and signaling mechanisms have not been fully elucidated. Our mass spectrometry-based screen of the gastrula secretome identified Admp as Pnhd-associated protein. We show that Pnhd binds Admp and inhibits its ventralizing activity by reducing Smad1 phosphorylation and its transcriptional targets. Importantly, Pnhd depletion further increased phospho-Smad1 levels in the presence of Admp. Furthermore, Pnhd synergized with Chordin and a truncated BMP4 receptor in the induction of notochord markers in ectoderm cells, and Pnhd-depleted embryos displayed notochord defects. Our findings suggest that Pnhd binds and inactivates Admp to promote notochord development. We propose that the interaction between Admp and Pnhd refines Smad1 activity gradients during vertebrate gastrulation.

	==2018==		==2018==

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 ===Frog Embryology===
 <pubmed limit=5>Frog Embryology</pubmed>
 ==2017==
 ===N1-Src kinase is required for primary neurogenesis in Xenopus tropicalis===

Z8600021 at 05:18, 12 August 2017

2017-08-12T05:18:39Z

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	==2017==		==2017==

			===N1-Src kinase is required for primary neurogenesis in Xenopus tropicalis===
			J Neurosci. 2017 Aug 1. pii: 3881-16. doi: 10.1523/JNEUROSCI.3881-16.2017. [Epub ahead of print]

			Lewis PA1, Bradley IC1, Pizzey AR1, Isaacs HV2, Evans GJO2.

			Abstract

			The presence of the neuronal-specific N1-Src splice variant of the C-Src tyrosine kinase is conserved through vertebrate evolution, suggesting an important role in complex nervous systems. Alternative splicing involving a N1-Src specific microexon leads to a five or six amino acid insertion into the SH3 domain of Src. A prevailing model suggests that N1-Src regulates neuronal differentiation via cytoskeletal dynamics in the growth cone. Here we have investigated the role of n1-src in the early development of the amphibian Xenopus tropicalis, and find that n1-src expression is regulated in embryogenesis, with highest levels detected during the phases of primary and secondary neurogenesis. In situ hybridisation analysis, using locked nucleic acid (LNA) oligo probes complementary to the n1-src microexon indicate that n1-src expression is highly enriched in the open neural plate during neurula stages and in the neural tissue of adult frogs. Given the n1-src expression pattern, we investigated a possible role for n1-src in neurogenesis. Using splice site-specific antisense morpholino oligos, we are able to inhibit n1-src splicing, whilst preserving c-src expression. Differentiation of neurons in the primary nervous system is reduced in n1-src knockdown embryos, accompanied by a severely impaired touch response in later development. These data reveal an essential role for n1-src in amphibian neural development and suggest that alternative splicing of C-Src in the developing vertebrate nervous system evolved to regulate neurogenesis.SIGNIFICANCE STATEMENTThe Src family of non-receptor tyrosine kinases act in signalling pathways that regulate cell migration, cell adhesion and proliferation. Srcs are also enriched in the brain where they play key roles in neuronal development and neurotransmission. Vertebrates have evolved a neuron-specific splice variant of C-Src, N1-Src, which differs from C-Src by just five or six amino acids. N1-Src is poorly understood and its high similarity to C-Src has made it difficult to delineate its function. Using antisense knockdown of the n1-src microexon, we have studied neuronal development in the Xenopus embryo in the absence of n1-src, whilst preserving c-src Loss of n1-src causes a striking absence of primary neurogenesis, implicating n1-src in the specification of neurons early in neural development.
			Copyright © 2017 Lewis et al.

			PMID: 28765332 DOI: 10.1523/JNEUROSCI.3881-16.2017


	===Endocrine disruption by environmental gestagens in amphibians - A short review supported by new in vitro data using gonads of Xenopus laevis===		===Endocrine disruption by environmental gestagens in amphibians - A short review supported by new in vitro data using gonads of Xenopus laevis===

Z8600021 at 00:49, 23 Mayıs 2017

2017-05-23T00:49:25Z

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	Amphibians; Endocrine disruption; Environmental gestagens; Gonads; Thyroid system		Amphibians; Endocrine disruption; Environmental gestagens; Gonads; Thyroid system
	PMID 28431277 DOI: 10.1016/j.chemosphere.2017.04.021		PMID 28431277 DOI: 10.1016/j.chemosphere.2017.04.021

			==2016==
			===Xenopus Limb bud morphogenesis===
			Dev Dyn. 2016 Mar;245(3):233-43. doi: 10.1002/dvdy.24351. Epub 2015 Nov 3.

			Keenan SR1, Beck CW1.

			Abstract

			Xenopus laevis, the South African clawed frog, is a well-established model organism for the study of developmental biology and regeneration due to its many advantages for both classical and molecular studies of patterning and morphogenesis. While contemporary studies of limb development tend to focus on models developed from the study of chicken and mouse embryos, there are also many classical studies of limb development in frogs. These include both fate and specification maps, that, due to their age, are perhaps not as widely known or cited as they should be. This has led to some inevitable misinterpretations- for example, it is often said that Xenopus limb buds have no apical ectodermal ridge, a morphological signalling centre located at the distal dorsal/ventral epithelial boundary and known to regulate limb bud outgrowth. These studies are valuable both from an evolutionary perspective, because amphibians diverged early from the amniote lineage, and from a developmental perspective, as amphibian limbs are capable of regeneration. Here, we describe Xenopus limb morphogenesis with reference to both classical and molecular studies, to create a clearer picture of what we know, and what is still mysterious, about this process.
			© 2015 Wiley Periodicals, Inc.

			KEYWORDS:
			amphibian; autopod; limb bud; mesoderm; morphogen; patterning; positional information; skeletal

			PMID 26404044 DOI: 10.1002/dvdy.24351

Z8600021 at 00:36, 23 Mayıs 2017

2017-05-23T00:36:23Z

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	===Frog Embryology===		===Frog Embryology===
	<pubmed limit=5>Frog Embryology</pubmed>		<pubmed limit=5>Frog Embryology</pubmed>

			==2017==

			===Endocrine disruption by environmental gestagens in amphibians - A short review supported by new in vitro data using gonads of Xenopus laevis===

			Chemosphere. 2017 Aug;181:74-82. doi: 10.1016/j.chemosphere.2017.04.021. Epub 2017 Apr 5.

			Ziková A1, Lorenz C2, Hoffmann F2, Kleiner W2, Lutz I2, Stöck M2, Kloas W3.

			Abstract

			Endocrine disruption caused by various anthropogenic compounds is of persisting concern, especially for aquatic wildlife, because surface waters are the main sink of these so-called endocrine disruptors (ED). In the past, research focused on (anti)estrogenic, (anti)androgenic, and (anti)thyroidal substances, affecting primarily reproduction and development in vertebrates; however, other endocrine systems might be also targeted by ED. Environmental gestagens, including natural progestogens (e.g. progesterone (P4)) and synthetic progestins used for contraception, are supposed to affect vertebrate reproduction via progesterone receptors. In the present paper, we review the current knowledge about gestagenic effects in amphibians, focussing on reproduction and the thyroid system. In addition, we support the literature data with results of recent in vitro experiments, demonstrating direct impacts of the gestagens levonorgestrel (LNG) and P4 on sexually differentiated gonads of larval Xenopus laevis. The results showed a higher susceptibility of female over male gonads to gestagenic ED. Only in female gonads LNG, but not P4, had direct inhibitory effects on gene expression of steroidogenic acute regulatory protein and P450 side chain cleavage enzyme, whereas aromatase expression decreased in reaction to both gestagens. Surprisingly, beyond the expected ED effects of gestagens on reproductive physiology in amphibians, LNG drastically disrupted the thyroid system, which resembles direct effects on thyroid glands and pituitary along the pituitary-thyroid axis disturbing metamorphic development. In amphibians, environmental gestagens not only affect the reproductive system but at least LNG can impact also development by disruption of the thyroid system.
			Copyright © 2017 Elsevier Ltd. All rights reserved.

			KEYWORDS:
			Amphibians; Endocrine disruption; Environmental gestagens; Gonads; Thyroid system
			PMID 28431277 DOI: 10.1016/j.chemosphere.2017.04.021

Z8600021 at 00:50, 30 August 2014

2014-08-30T00:50:46Z

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 PMID 24204686
 ==2012==
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 :"How embryos consistently orient asymmetries of the left-right (LR) axis is an intriguing question, as no macroscopic environmental cues reliably distinguish left from right. Especially unclear are the events coordinating LR patterning with the establishment of the dorsoventral (DV) axes and midline determination in early embryos. In frog embryos, consistent physiological and molecular asymmetries manifest by the second cell cleavage; however, models based on extracellular fluid flow at the node predict correct de novo asymmetry orientation during neurulation. We addressed these issues in Xenopus embryos by manipulating the timing and location of dorsal organizer induction: the primary dorsal organizer was ablated by UV irradiation, and a new organizer was induced at various locations, either early, by mechanical rotation, or late, by injection of lithium chloride (at 32 cells) or of the transcription factor XSiamois (which functions after mid-blastula transition). These embryos were then analyzed for the position of three asymmetric organs. Whereas organizers rescued before cleavage properly oriented the LR axis 90% of the time, organizers induced in any position at any time after the 32-cell stage exhibited randomized laterality. Late organizers were unable to correctly orient the LR axis even when placed back in their endogenous location. Strikingly, conjoined twins produced by late induction of ectopic organizers did have normal asymmetry. These data reveal that although correct LR orientation must occur no later than early cleavage stages in singleton embryos, a novel instructive influence from an early organizer can impose normal asymmetry upon late organizers in the same cell field."
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 PMID 7505061

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	During early vertebrate development, epithelial cells establish and maintain apicobasal polarity, failure of which can cause developmental defects or cancer metastasis. This process has been mostly studied in simple epithelia that have only one layer of cells, but is poorly understood in stratified epithelia. In this paper we address the role of the polarity protein Partitioning defective-6 homolog beta (Par6b) in the developing stratified epidermis of Xenopus laevis. At the blastula stage, animal blastomeres divide perpendicularly to the apicobasal axis to generate partially polarized superficial cells and non-polarized deep cells. Both cell populations modify their apicobasal polarity during the gastrula stage, before differentiating into the superficial and deep layers of epidermis. Early differentiation of the epidermis is normal in Par6b-depleted embryos; however, epidermal cells dissociate and detach from embryos at the tailbud stage. Par6b-depleted epidermal cells exhibit a significant reduction in basolaterally localized E-cadherin. Examination of the apical marker Crumbs homolog 3 (Crb3) and the basolateral marker Lethal giant larvae 2 (Lgl2) after Par6b depletion reveals that Par6b cell-autonomously regulates the dynamics of apicobasal polarity in both superficial and deep epidermal layers. Par6b is required to maintain the "basolateral" state in both epidermal layers, which explains the reduction of basolateral adhesion complexes and epidermal cells shedding.		During early vertebrate development, epithelial cells establish and maintain apicobasal polarity, failure of which can cause developmental defects or cancer metastasis. This process has been mostly studied in simple epithelia that have only one layer of cells, but is poorly understood in stratified epithelia. In this paper we address the role of the polarity protein Partitioning defective-6 homolog beta (Par6b) in the developing stratified epidermis of Xenopus laevis. At the blastula stage, animal blastomeres divide perpendicularly to the apicobasal axis to generate partially polarized superficial cells and non-polarized deep cells. Both cell populations modify their apicobasal polarity during the gastrula stage, before differentiating into the superficial and deep layers of epidermis. Early differentiation of the epidermis is normal in Par6b-depleted embryos; however, epidermal cells dissociate and detach from embryos at the tailbud stage. Par6b-depleted epidermal cells exhibit a significant reduction in basolaterally localized E-cadherin. Examination of the apical marker Crumbs homolog 3 (Crb3) and the basolateral marker Lethal giant larvae 2 (Lgl2) after Par6b depletion reveals that Par6b cell-autonomously regulates the dynamics of apicobasal polarity in both superficial and deep epidermal layers. Par6b is required to maintain the "basolateral" state in both epidermal layers, which explains the reduction of basolateral adhesion complexes and epidermal cells shedding.
			PMID 24204686

			==2013==

			===Par6b regulates the dynamics of apicobasal polarity during development of the stratified Xenopus epidermis===
			PLoS One. 2013 Oct 18;8(10):e76854. doi: 10.1371/journal.pone.0076854. eCollection 2013.

			Wang S1, Cha SW, Zorn AM, Wylie C.

			Abstract

			During early vertebrate development, epithelial cells establish and maintain apicobasal polarity, failure of which can cause developmental defects or cancer metastasis. This process has been mostly studied in simple epithelia that have only one layer of cells, but is poorly understood in stratified epithelia. In this paper we address the role of the polarity protein Partitioning defective-6 homolog beta (Par6b) in the developing stratified epidermis of Xenopus laevis. At the blastula stage, animal blastomeres divide perpendicularly to the apicobasal axis to generate partially polarized superficial cells and non-polarized deep cells. Both cell populations modify their apicobasal polarity during the gastrula stage, before differentiating into the superficial and deep layers of epidermis. Early differentiation of the epidermis is normal in Par6b-depleted embryos; however, epidermal cells dissociate and detach from embryos at the tailbud stage. Par6b-depleted epidermal cells exhibit a significant reduction in basolaterally localized E-cadherin. Examination of the apical marker Crumbs homolog 3 (Crb3) and the basolateral marker Lethal giant larvae 2 (Lgl2) after Par6b depletion reveals that Par6b cell-autonomously regulates the dynamics of apicobasal polarity in both superficial and deep epidermal layers. Par6b is required to maintain the "basolateral" state in both epidermal layers, which explains the reduction of basolateral adhesion complexes and epidermal cells shedding.

	PMID 24204686		PMID 24204686

Z8600021 at 00:33, 30 August 2014

2014-08-30T00:33:06Z

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	<pubmed limit=5>Frog Embryology</pubmed>		<pubmed limit=5>Frog Embryology</pubmed>


			==2014==

			===Par6b regulates the dynamics of apicobasal polarity during development of the stratified Xenopus epidermis===
			PLoS One. 2013 Oct 18;8(10):e76854. doi: 10.1371/journal.pone.0076854. eCollection 2013.

			Wang S1, Cha SW, Zorn AM, Wylie C.

			Abstract

			During early vertebrate development, epithelial cells establish and maintain apicobasal polarity, failure of which can cause developmental defects or cancer metastasis. This process has been mostly studied in simple epithelia that have only one layer of cells, but is poorly understood in stratified epithelia. In this paper we address the role of the polarity protein Partitioning defective-6 homolog beta (Par6b) in the developing stratified epidermis of Xenopus laevis. At the blastula stage, animal blastomeres divide perpendicularly to the apicobasal axis to generate partially polarized superficial cells and non-polarized deep cells. Both cell populations modify their apicobasal polarity during the gastrula stage, before differentiating into the superficial and deep layers of epidermis. Early differentiation of the epidermis is normal in Par6b-depleted embryos; however, epidermal cells dissociate and detach from embryos at the tailbud stage. Par6b-depleted epidermal cells exhibit a significant reduction in basolaterally localized E-cadherin. Examination of the apical marker Crumbs homolog 3 (Crb3) and the basolateral marker Lethal giant larvae 2 (Lgl2) after Par6b depletion reveals that Par6b cell-autonomously regulates the dynamics of apicobasal polarity in both superficial and deep epidermal layers. Par6b is required to maintain the "basolateral" state in both epidermal layers, which explains the reduction of basolateral adhesion complexes and epidermal cells shedding.
			PMID 24204686

	==2012==		==2012==

Z8600021 at 03:01, 4 April 2013

2013-04-04T03:01:46Z

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	* '''Thyroid hormone-dependent metamorphosis in a direct developing frog'''. Callery, EM and Elinson RP, Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 6, 2615-2620, March 14, 2000		* '''Thyroid hormone-dependent metamorphosis in a direct developing frog'''. Callery, EM and Elinson RP, Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 6, 2615-2620, March 14, 2000
	** The direct developing anuran, Eleutherodactylus coqui, lacks a tadpole, hatching as a tiny frog. We investigated the role of the metamorphic trigger, thyroid hormone (TH), in this unusual ontogeny. Expression patterns of the thyroid hormone receptors, TR and TR, were similar to those of indirect developers. TR mRNA levels increased dramatically around the time of thyroid maturation, when remodeling events reminiscent of metamorphosis occur. Treatment with the goitrogen methimazole inhibited this remodeling, which was reinitiated on cotreatment with TH. Despite their radically altered ontogeny, direct developers still undergo a TH-dependent metamorphosis, which occurs before hatching. We propose a new model for the evolution of anuran direct development.		** The direct developing anuran, Eleutherodactylus coqui, lacks a tadpole, hatching as a tiny frog. We investigated the role of the metamorphic trigger, thyroid hormone (TH), in this unusual ontogeny. Expression patterns of the thyroid hormone receptors, TR and TR, were similar to those of indirect developers. TR mRNA levels increased dramatically around the time of thyroid maturation, when remodeling events reminiscent of metamorphosis occur. Treatment with the goitrogen methimazole inhibited this remodeling, which was reinitiated on cotreatment with TH. Despite their radically altered ontogeny, direct developers still undergo a TH-dependent metamorphosis, which occurs before hatching. We propose a new model for the evolution of anuran direct development.

			==Historic==

			On the Structure and Development of the Skull of the Common Frog (Rana temporaria, L.) (January 1, 1871) http://archive.org/details/philtrans05966609

			On the Development of the Teeth of the Newt, the Frog, and Certain Lizards. (January 1, 1874)
			http://archive.org/details/philtrans03024546

			The frog; its reproduction and development (1951)
			http://archive.org/details/frogitsreproduct00rugh

			Some Experiments on the Development and Regeneration of the Eye and the Nasal Organ in Frog Embryos (February 1, 1908)
			http://archive.org/details/jstor-2455263

Z8600021 at 20:05, 24 December 2012

2012-12-24T20:05:39Z

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	===Frog Development===		===Frog Development===
	<pubmed limit=10>Frog Development</pubmed>		<pubmed limit=5>Frog Development</pubmed>

			===Frog Embryology===
			<pubmed limit=5>Frog Embryology</pubmed>