i want complete explanation about development of frog-[from gamete formation, cleavage and blastulation, fate map, gastulation to metamorphosis ] in about 300-350 words
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The frog has been historically been used as an amphibian animal model of development due to the ease of observation from the fertilized egg through to tadpole stage. The later metamorphosis of the tadpole to frog has also been studied for hormonal controls and limb development. There have also been many different species used in these developmental studies.
The frog was historically used by many of the early embryology investigators and currently there are many different molecular mechanisms concerning development of the frog. The 2012 Nobel prize in medicine was recently awarded to John Gurdon for his 1960's experiments involving nuclear transplantation with adult nuclei into frog eggs, these studies were the precursor to current research in stem cells.
The African clawed frog (Xenopus laevis) has been used in many embryological and electrophysiological studies as well as the basis of a historic pregnancy test. The advantages of this frog is the fertility cycle can be easliy controlled and the eggs develop entirely independently and easily visible to the investigator. You can see an overview of the frog life cycle with links to specific stages as well as movies of the early process of gastrulation. This animal model has also shown that localization of maternal messenger RNA (eg vegetal and review) appears to play a key role in the development of early embryological patterns.
The Leopard frog (Rana pipiens) in 1952 became the first successful nuclear transfer experiment. Nuclear transfer is an embryological technique, and involves removal of the nucleus from an egg and replacement with the nucleus of another donor cell. This experiment paved the way for what we know today as the field of cloning.[1]
In Australia, the cane toad (Bufo marinus) species was introduced in 1935 to control cane insect pests. It has now itself become an introduced pest and has also been studied/used more in order to try and biologically control. The area which they occupy has continued to expand. This toad has a poisonous secretion that is extremely toxic and should be handled with care at all times.
Anosmin-1 is essential for neural crest and cranial placodes formation in Xenopus[3] "During embryogenesis vertebrates develop a complex craniofacial skeleton associated with sensory organs. These structures are primarily derived from two embryonic cell populations the neural crest and cranial placodes, respectively. ...Anos1 was identified as a target of Pax3 and Zic1, two transcription factors necessary and sufficient to generate neural crest and cranial placodes. Anos1 is expressed in cranial neural crest progenitors at early neurula stage and in cranial placode derivatives later in development. We show that Anos1 function is required for neural crest and sensory organs development in Xenopus, consistent with the defects observed in Kallmann syndrome patients carrying a mutation in ANOS1."
EphA7 regulates claudin6 and pronephros development in Xenopus[4] "Here we studied the roles of the Eph receptor EphA7 and its soluble form in Xenopus pronephros development. EphA7 is specifically expressed in pronephric tubules at tadpole stages and knockdown of EphA7 by a translation blocking morpholino led to defects in tubule cell differentiation and morphogenesis. A soluble form of EphA7 (sEphA7) was also identified. ...Our work suggests a role of EphA7 in the regulation of cell adhesion during pronephros development, whereas sEphA7 works as an antagonist."
N1-Src kinase is required for primary neurogenesis in Xenopus tropicalis[5] "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. The 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." Neural System Development
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