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Prokaryotes possess a nucleus whereas eukaryotes do not, but eukaryotes show greater compartmentalization that allows for greater regulation of gene expression.
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Eukaryotic cells contain a nucleus whereas prokaryotes do not, and eukaryotes show greater compartmentalization that allows for greater regulation of gene expression.
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Prokaryotic cells are less complex and perform highly-regulated gene expression whereas eukaryotes perform less-regulated gene expression.
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Eukaryotic cells are more complex and perform less-regulated gene expression whereas prokaryotic cells perform highly-regulated gene expression.
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Prokaryotes regulate gene expression at the level of transcription whereas eukaryotes regulate at multiple levels including epigenetic, transcriptional and translational.
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Prokaryotes regulate gene expression at the level of translation whereas eukaryotes regulate at the level of transcription to manipulate protein levels.
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Prokaryotes regulate gene expression with the help of repressors and activators whereas eukaryotes regulate expression by degrading mRNA transcripts, thereby controlling protein levels.
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Prokaryotes control protein levels using epigenetic modifications whereas eukaryotes control protein levels by regulating the rate of transcription and translation.
All the cells of one organisms share the genome. However, during development, some cells develop into skin cells while others develop into muscle cells. How can the same genetic instructions result in two different cell types in the same organism? Thoroughly explain your answer.
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When lactose and glucose are present in the medium, transcription of the lac operon is induced.
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When lactose is present but glucose is absent, the lac operon is repressed.
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Lactose acts as an inducer of the lac operon when glucose is absent.
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Lactose acts as an inducer of the lac operon when glucose is present.
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Mutation in structural genes will stop transcription.
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Mutated lacY will prevent CAP from binding.
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Mutated lacA will metabolize lactose or maltodextrin.
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Transcription will continue but lactose will not be metabolized properly.
In some diseases, alteration to epigenetic modifications turns off genes that are normally expressed. Hypothetically, how could you reverse this process to turn these genes back on?
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In new seedlings, histone acetylations are present; upon cold exposure, methylation occurs.
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In new seedlings, histone deacetylations are present; upon cold exposure, methylation occurs.
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In new seedlings, histone methylations are present; upon cold exposure, acetylation occurs.
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In new seedlings, histone methylations are present; upon cold exposure, deacetylation occurs.
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Mutated promoters decrease the rate of transcription by altering the binding site for the transcription factor.
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Mutated promoters increase the rate of transcription by altering the binding site for the transcription factor.
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Mutated promoters alter the binding site for transcription factors to increase or decrease the rate of transcription.
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Mutated promoters alter the binding site for transcription factors and thereby cease transcription of the adjacent gene.
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The transcription rate would increase, altering cell function.
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The transcription rate would decrease, inhibiting cell functions.
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The transcription rate decreases due to clogging of the transcription factors.
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The transcription rate increases due to clogging of the transcription factors.
The wnt transcription pathway is responsible for key changes during animal development. Based on the transcription pathway shown below. In this diagram, arrows indicate the transformation of one substance into another. Square lines, or the lines with no arrowheads, indicate inhibition of the product below the line. Based on this, how would increased wnt gene expression affect the expression of Bar-1?
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RBPs can bind first to the RNA, thus preventing the binding of miRNA, which degrades RNA.
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RBPs bind the miRNA, thereby protecting the mRNA from degradation.
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RBPs methylate miRNA to inhibit its function and thus stop mRNA degradation.
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RBPs direct miRNA degradation with the help of a DICER protein complex.
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UV rays can alter methylation and acetylation of proteins.
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RNA binding proteins are modified through phosphorylation.
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External stimuli can cause deacetylation and demethylation of the transcript.
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UV rays can cause dimerization of the RNA binding proteins.
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Phosphorylation of proteins can alter translation, RNA shuttling, RNA stability or post transcriptional modification.
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Phosphorylation of proteins can alter DNA replication, cell division, pathogen recognition and RNA stability.
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Phosphorylated proteins affect only translation and can cause cancer by altering the p53 function.
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Phosphorylated proteins affect only RNA shuttling, RNA stability, and post-translational modifications.
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UV rays could cause methylation and deacetylation of the genes that could alter the accessibility and transcription of DNA.
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The UV rays could cause phosphorylation and acetylation of the DNA and histones which could alter the transcriptional capabilities of the DNA.
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UV rays could cause methylation and phosphorylation of the DNA bases which could become dimerized rendering no accessibility of DNA.
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The UV rays can cause methylation and acetylation of histones making the DNA more tightly packed and leading to inaccessibility.
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These drugs maintain the demethylated and the acetylated forms of the DNA to keep transcription of necessary genes “on”.
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The demethylated and the acetylated forms of the DNA are reversed when the silenced gene is expressed.
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The drug methylates and acetylates the silenced genes to turn them back “on”.
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Drugs maintain DNA methylation and acetylation to silence unimportant genes in cancer cells.
The graphs shows the tumor-suppressor gene, p53, and its mutations detected in cancer patients. The x-axis is the codon number of the gene. The y-axis is the frequency a mutation is detected in that codon.
What is a conclusion we can draw from this graph?
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Mutations in the central region of the gene are more likely to cause cancer.
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Mutations in the beggining parts of the gene are more likely to cause cancer.
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The mutations are evenly distributed among the codons.
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The mutations are concentrated in 5 codons. Mutations in other codons does not increase risk of cancer.
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Personalized medicines would vary based on the type of mutations and the gene’s expression pattern.
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The medicines are given based on the type of tumor found in the body of an individual.
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The personalized medicines are provided based only on the symptoms of the patient.
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The medicines tend to vary depending on the severity and the stage of the cancer.