Concept explainers
To analyze:
Introduction:
In bioinformatics, BLAST stands for “basic local alignment search tool” that finds the region of local similarity between biological sequences. This algorithm compares a DNA sequence or an amino acid sequence to the sequences that are in the databases and calculates the statistical significance of the sequence matches. There are different types of BLAST presently used according to the query sequence. One of the BLAST types, tblastn can be used to find the homologous gene sequence for the predicted sequence of
Want to see the full answer?
Check out a sample textbook solutionChapter 16 Solutions
Pearson eText Genetic Analysis: An Integrated Approach -- Instant Access (Pearson+)
- The Saccharomyces cerevisiae nuclear gene ARG8encodes an enzyme that catalyzes a key step in biosynthesis of the amino acid arginine. This protein isnormally synthesized on cytoplasmic ribosomes, butthen is transported into mitochondria, where the enzyme conducts its functions. In 1996, T. D. Fox andhis colleagues constructed a strain of yeast in which agene encoding the Arg8 protein was itself moved intomitochondria, where functional protein could besynthesized on mitochondrial ribosomes.a. How could these investigators move the ARG8gene from the nucleus into the mitochondria, whilepermitting the synthesis of active enzyme? In whatways would the investigators need to alter theARG8 gene to allow it to function in the mitochondria instead of in the nucleus?b. Why might these researchers have wished to movethe ARG8 gene into mitochondria in the firstplace?arrow_forwardLeber Congenital Amaurosis (LCA) causes progressive vision loss due to defects in the gene that encodes RPE65 isomerase. Affected individuals are homozygous recessive for mutant alleles of the RPE65 gene. You are trying to determine the molecular nature of the mutations in three individuals with LCA. For ease of analysis, you may assume that each individual is homozygous for the same mutant allele (though the three individuals have different mutations than each other). You use the polymerase chain reaction to amplify DNA from each patient and you determine the sequence of the DNA and compare it to unaffected individuals. You identify the following differences. Note that the non-template strand of DNA is given and the changes are highlighted using red boldface. You can assume that the sequences are in the first reading frame (eg. the first three nucleotides of each sequence is a codon). The coding region of the gene is 1602 bp and the position of the sequences shown below is…arrow_forwardThe chromosomal sequences of two mutant alleles of gene A from patients with the zero subtype include the following mutation: 496G>A. Briefly discuss why this mutant fails to produce a functional protein. Note that none of the mRNA transcribed from this gene is of the expected size; some of the mRNA molecules produced are 223 nucleotides shorter than expected whilst others are 47 nucleotides longer than expected. The mutation on position 496 is highlighted in yellow, this will become A instead of G. However, it is the start of an intron, therefore the mutation won't affect the protein. but the question implies that the mutation will affect the protein.arrow_forward
- Mice usually have wild-type agouti fur that appears grey, but a mouse geneticist has a pure-breeding white-furred strain that is homozygous for a recessive mutation. Molecular analysis shows that the mutation is a missense mutation in an exon common to three alternatively spliced forms of a gene expressed in hair follicles. Which of the following transgenic animals would be most useful to determine which spliced form (or forms) is sufficient to specify agouti fur?A. Construct a GFP reporter using the promoter for the identified gene. B. Express a wild-type version of a cDNA for each spliced form in the white mutant mouse to see which form(s) rescue the phenotype. C. Use CRISPR/Cas9 to make a large deletion of the entire coding region of the identified gene. D. Introduce the wild-type genomic allele into the mutant mouse to test for rescue of the mutant phenotypearrow_forwardIn a mutant mouse, it was discovered that a gene "W" is moved from its original chromosomal locus to the telomere region, where chromatin is packed into heterochromatin. Given what we have learned about eukaryotic gene regulation, can you speculate how the expression of gene W in the new mouse line would be changed as compare to the normal mouse? elevated in the mutant mouse than in the wild-type mouse. cannot be determined. O reduced in the mutant mouse than in the wild-type mouse. change in the mutant mouse as compared to the wild-type mouse.arrow_forwardGene A, which encodes alcohol dehydrogenase, is labeled with a red fluorophore in a FISH experiment with one chromosome of a homologous pair, with results shown below. Gene B is labeled in green and encodes Notch2NL, a gene which may help to explain brain size differences between humans and chimpanzees, and which with increased dosage, may lead to a condition referred to as macrocephaly (enlarged head circumference sometimes associated with learning disabilities). What can you infer about these two genes given the results seen below?arrow_forward
- The D1S80 locus is located on human chromosome 1 and is characterized by a repeating 16 base pair (bp) sequence. Alleles for this locus vary depending on the number of repeats present, thus affecting the size of the locus. The D1S80 locus also contains two conserved sequences, a 32bp sequence at one end and a 113bp sequence at the other end. If the DNA of an individual is targeted for D1S80 amplification, and one of the resulting amplicons is approximately 785bp in size, how many repeats would be present in this D1S80 allele? The amplicon of interest is indicated by a red arrow in the diagram below.arrow_forwardUsing a transgenic technique, propose an experiment to determine whether Cdx2 is sufficient for trophoblast development in the mouse embryo. Describe two results that you would expect to observe at the blastocyst stage if Cdx2 is indeed sufficient for trophoblast development. Be as specific as possible regarding the transgene that you propose for this experiment (including what gene's enhancer you would use in the transgene). Note: you do not need to explain the details of how a transgenic mouse is made. Describe the experiment in steps (Step 1: ..., Step 2: ... etc) and please keep your answer to under 150 words. tips: DONT talk about stop cassetes/memory cassetes, focus on transgenes Paper called "Cdx2 is required for correct cell fate specification and differentiation of trophectoderm in the mouse blastocyst" gave lots of results that you might see,, 6 diff ways that cdx2 is required for trophoblasts need specific gene enhancer (dont just say "expressed enhancer in genital…arrow_forwardIn a mutant mouse, it was discovered that a gene "W" is moved from its original chromosomal locus to the telomere region, where chromatin is packed into heterochromatin. Given what we have learned about eukaryotic gene regulation, can you speculate how the expression of gene W in the new mouse line would be changed as compare to the normal mouse? Question 18 options: elevated in the mutant mouse than in the wild-type mouse. cannot be determined. reduced in the mutant mouse than in the wild-type mouse. no change in the mutant mouse as compared to the wild-type mouse.arrow_forward
- Lysine 4 of histone H3 (H3K4) is methylated in thenucleosomes of many transcriptionally active genes.Suppose you want to determine all the places in thehuman genome where nucleosomes contain methylated H3K4.a. Starting with an antibody that specifically bindsonly to the tails of histone H3s that have K4 methylation, what kind of experiment would you perform? Outline the major steps of this experiment.b. Do you think that you would get the same results ifyour starting material was skin cells in one experiment and blood precursor cells in a second experiment? Explain.c. Describe a follow-up experiment that could determine if your data from part (a) are consistent withthe idea that H3K4 methylation marks appear onlyat transcriptionally active genesarrow_forwardDifferent mutations in the WDR62 gene that inactivate gene function were found in the genomes of many different people with microcephaly. This information provided strong support for the idea that the WDR62 gene mutation causes microcephaly. The human genome sequence identified WDR62 as one of the approximately 27,000 genes in the human genome. What information about the function of WDR62 do you think was learned originally from the DNA sequence of the normal human genome? What additional information was provided by identification of WDR62 as the microcephaly disease gene?arrow_forwardthis is what i have said about this image so far, what else can be said aswell including the raw count column. " Interpreting the results of an RNA-Seq analysis is pivotal in understanding the underlying genetic mechanisms of diseases such as breast cancer. In this analysis, Figure 1 provides comprehensive data on differentially expressed genes associated with breast cancer. By delving into the provided information, we can gain valuable insights into the molecular landscape of this disease. First focus is on the gene with the highest fold change, EYA4, situated on chromosome 6. With a staggering fold change of 3604.4176, EYA4 exhibits an unprecedented level of overexpression in cancerous cells compared to normal cells. This profound alteration suggests a pivotal role for EYA4 in breast cancer pathogenesis. The log2 fold change of 11.81555 further emphasizes the magnitude of this difference in gene expression. Statistical significance is evident, with an exceptionally low p-value of…arrow_forward
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education