Use Ch. 12, 16-19 in \"Campbell Biology\" Pearson book by Urry, Cain, Wasserman,

Question

Use Ch. 12, 16-19 in "Campbell Biology" Pearson book by Urry, Cain, Wasserman, Minorsky, and Reece. Write in multiple paragraph form. Please be detailed. Include vocabulary and concepts listed below question.

1) Diagram and describe the process of DNA replication. [Hints: Be sure to explain why there are leading and lagging strands. This will be easier if you draw an entire replication bubble, and show how it changes in size as replication proceeds. Your answer should also include the ends of eukaryotic chromosomes.]

Important Concepts

DNA structure & replication

DNA structure: What parts are the same for all the nucleotides? What parts are different? What’s the structural difference between RNA and DNA? Show what antiparallel & complementary mean.

DNA serves as a template for making DNA & RNA

Origin of replication, replication fork, replication bubble. Draw a diagram showing how these relate to each other. Remember that the replication fork diagrams in the book aren’t showing the ends of the DNA molecule – just one side of a replication bubble.

5’, 3’. Diagram the 5’ and 3’ ends of template DNA, primers, and newly synthesized DNA. Why are new nucleotides added only at the 3’ end?

Primase & primer. Compare DNA synthesis to transcription in terms of priming. How is priming in PCR different from priming in cellular DNA synthesis?

Topoisomerase, helicase, & single-strand binding protein

DNA polymerases. Why is there more than one kind?

DNA ligase. Do eukaryotes need it? Do prokaryotes need it?

Leading & lagging; Okazaki fragments. Why are the two ends different? Be sure to diagram this in terms of a whole replication bubble – not just a replication fork.

End-replication problem; telomeres & telomerase. Which strand gets extended by telomerase? How does this help solve the end-replication problem? Study the diagrams. Which cells have telomerase, and which don’t?

Genes & gene expression

What is a gene? What is a transcription unit? Does one gene always code for one protein?
Genome sizes. What does the graph represent? How could an organism with a more complex body have a smaller genome than an organism with a simpler body?

Chimpanzees and humans: how different are the genomes? Why is this question hard to answer? What makes chimpanzees different from humans – different proteins? Different genes?

Translation:

Genetic code; codon. How many codons are there? How many code for amino acids? What do the others do? What is the genetic code?

tRNA; anticodon; aminoacyl-tRNA synthetase. What key role do aminoacyl-tRNA synthetases play in translation? Why is there more than one?

Ribosome structure. What are ribosomes made of? Where are they made? Why are there 3 tRNA binding sites?

Translation initiation complex

Why wouldn't a transcribed mRNA not be translated immediately?

Elongation & translocation in translation. In translocation, which parts move relative to one another, and which don’t?

Termination; release factor

Bacterial operons & regulating metabolic pathways

Two kinds of control: enzyme regulation vs. gene regulation. Why?

trp operon. How does the presence of tryptophan prevent the synthesis of more tryptophan (2 different ways)?

lac operon. Compare & contrast with trp.

Why are operons for catabolic and anabolic pathways regulated differently?

Positive vs. negative gene regulation. Why would both be used for the same operon?

AraC mechanism. Is AraC an inducer or a repressor?

Eukaryotic gene regulation: transcription initiation

Initiation & the transcription initiation complex (including enhancers).

Promoter; TATA box; Conserved & variable regions in promoters.

Eukaryotic enhancers. Why is it important that there are multiple control elements in a single enhancer? What binds to the control elements? How is it possible for a small number of activator and transcription factor proteins to regulate a large number of genes?

Transcription: Elongation & RNA polymerase. RNA polymerase vs. DNA polymerase. Termination.

MyoD: What makes it a master regulator of differentiation? What genes does MyoD regulate? How is muscle differentiation related to cell proliferation?

Homeobox genes. How do they regulate other genes? Why are they so important for animals?

Eukaryotic gene regulation: Epigenetic factors

Chromatin structure: histones, methylation; euchromatin vs. heterochromatin. How does all this affect transcription?

X chromosome inactivation. Why does it happen? How does it happen? How does it result in calico cats? What does Xist do?

Heritable, but can be modified by environment… what does this mean?

Prader-Willi syndrome vs. Angelman syndrome: compare and contrast.

microRNAs. How are they different from mRNAs? How do they interact with mRNAs? How are microRNAs different from Xist or other long noncoding RNAs?

Post-transcriptional modification of RNA

Introns & exons. Which groups of organisms have introns? What is the evolutionary and functional significance of this? What happens to the introns?

Spliceosome

Alternative splicing; exons & domains.

5’ Cap, 3’ poly-A tail. How does this help regulate gene expression?

Pre-mRNA vs. mRNA

How is it possible for the total number of proteins in the proteome to be larger than the total number of protein-coding genes in the genome?

Post-translational modification

Protein targeting to ER & elsewhere; signal peptide & signal recognition particle. Why are some proteins targeted to the ER? Compare secreted proteins to integral membrane proteins.

Free vs. bound ribosomes

How is the control of gene expression different in prokaryotes & eukaryotes?

Mutations

Point mutations: substitution, insertion, deletion.

Mutation effects: silent, missense, nonsense. Frameshift.

The Cell Cycle

What does "cell cycle" mean? How does mitosis relate to the cell cycle?

Binary fission in bacteria. Why don’t prokaryotes do mitosis?

Interphase: G0, G1, S, G2

Mitosis stages: Prophase, metaphase, anaphase, telophase

Homologous chromosomes. When are they present?

Sister chromatids. When are they present?

Spindle, centrosome, centriole, microtubule, centromere, kinetochore

Cytokinesis. Compare animals to plants.

Checkpoints

G1, G2, M checkpoints: What gets checked at each checkpoint?

Cyclin & Cdk. What does Cdk do? Why does cyclin get destroyed? Why is there more than one kind of cyclin & Cdk? How does DNA damage affect Cdk/Cyclin? How do growth factor signaling pathways affect Cdk/Cyclin?

p53 protein and its multiple functions.

What happens to cells that don’t pass checkpoints?

Apoptosis

Role of mitochondria in apoptosis. Mitochondrial outer membrane permeabilization and cytochrome C.

Cell death proteins; pathways for inducing apoptosis. Why so much redundancy?

Senescence & telomeres

What kinds of organisms have senescence? What kinds of organisms have telomeres? Do these things always go together? If a cell has telomeres, does it have telomerase?

Cancer Biology

Characteristics of cancer cells. Consider the roles of: growth signals, stop signals, apoptosis, angiogenesis, immortality, metastasis

Why a tumor isn’t a clone

Oncogenes & proto-oncogenes. Why do they normally exist in the cell? Are the dangerous mutations loss-of-function or gain-of-function? Dominant or recessive?

Tumor suppressors. Why do they normally exist in the cell? Are the dangerous mutations loss-of-function or gain-of-function? Dominant or recessive?

p53. It does more than one thing. Why are changes in particular regions of the p53 protein most likely to cause problems? How is p53 connected to telomere shortening and proliferative senescence?

Why does carcinogenesis always require more than one genetic change?

How can a virus cause cancer?

Chromosome integrity. How might this be affected by loss of telomeres?

Chronic myelogenous leukemia, translocation, and the Bcr/Abl fusion protein. What is a “rationally designed drug?”

Aneuploidy and cancer. Changes in gene sequence vs. changes in gene dosage. What sorts of mutations could lead to aneuploidy?

How can a cancer be caused by epigenetic changes in a cell? How are epigenetic changes different from genetic changes? How can genetic mutations cause epigenetic changes?

Stem cells and cancer. How are cancer cells like stem cells? How are they different?

Explanation / Answer

Please find the answers below:

Answer 1:

Part 1: What parts are the same for all the nucleotides?

Answer: The nucleotide represents to be the structural unit of nucleic acid and contains three parts, similar to DNA as well as RNA:

Part 2: What parts are different?

Answer: The parts different in nucleotides are as enlisted below:

Part 3: What’s the structural difference between RNA and DNA?

Answer: The structural difference between DNA and RNA can be enlisted as below:

Part 4: Show what antiparallel & complementary mean.

Answer: The anti-parallele property of nucleic acids refers to the opposite chirality of the two strands of the nucleic acid, each maintaining its own directionality. This means that whereas one strand of the DNA serves as the 3' to 5' end, the other will have anti-parallel composition in the 5' to 3' direction.

Complementarity refers to the ability of DNA or RNA to bind or synthesize to chemically compatible nitrogenous bases. According to this rule, a purine always binds complementarily with a pyrimidine by a fixed number of hydrogen bonds. For example, an adenine binds always to thymidine or uracil and a cytosine always binds to a guanine base.

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