Based on the BLASTp and Reciprocal hit analysis is mus musculus a true ortholog for the human fgfr3 gene?

How can one most effectively silence the myofilament gene unc-22 in C. elegans to produce the twitching phenotype? O A. Screen thousands of strains for a spontaneous unc-22 mutation O B. Soak worms in mutagenic solutions of EMS and screen the progeny OC. Inject antisense strands of unc-22 RNA into worm ovaries, which will be taken up by germ line cells and expressed in progeny O D. Inject a high dose of unc-22 MRNA into worm ovaries, which will be taken up by germ line cells and expressed in progeny O E. Culture worms with E. coli transformed with a plasmid that codes for a dsRNA unc-22 construct

Describe the mechanism of genomic imprinting of the Igf2 gene in mammals.

Based on Pruisner (2013), match each of the following terms with its appropriate definition or description.                                                                         PRNP gene                                                                        CPEB (cytoplasmic polyadenylation element binding) protein                                                                        NFT (neurofibrillary tangle)                                                                        A673T-mutated AAP                                                                        MAPT gene A. a "nonpathogenic prion" B. encodes PrPC (the normal cellular form of prion protein) C. encodes tau protein;  mutations in this gene underlie many familial FTDs (frontotemporal dementias) D. tau-rich fibril associated with many neurodegenerative diseases E. a missense mutation in β-secretase which appears to protect against late-onset…

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Explain the signaling mechanism of retinoic acid, the source of retinoic acid in vivo, and how retinoic acid is important for the anteroposterior pattern of Hox gene expression?

how this stuttering mechanism can change the number of repeat units at theSSR locus responsible for Huntington disease?

Briefly explain the regulatory interactions between these three classes of patterning genes (gap, pair rule, segment polarity).  What is the temporal order of action and how do the different classes of genes regulate each other?

What would be the most likely result of injecting bicoid mRNA into the posterior end of a Drosophila embryo and inhibiting the translation of nanos mRNA?

What is the structural difference between normal EGFR and oncogenic receptor, e.g. ERbB? How does it affect its activity?