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What is the name of the method developed by Fred Sanger to sequence DNA? a. Dideoxy Chain Termination method b. Double Helix Determination c. Polymerase Chain Reaction d. Polymer Gel Electrophoresis

Short Answer

Expert verified
a. Dideoxy Chain Termination method

Step by step solution

01

- Understanding the Options Given

Read through each of the given options carefully: a. Dideoxy Chain Termination method b. Double Helix Determination c. Polymerase Chain Reaction d. Polymer Gel Electrophoresis
02

- Identifying Relevant Scientific Discoveries

Recall that Fred Sanger is famous for his contributions to DNA sequencing.
03

- Matching the Method to the Scientist

Remember that the method developed by Fred Sanger for DNA sequencing is specifically known for its use of dideoxynucleotides to terminate DNA synthesis.
04

- Choosing the Correct Answer

From the options given, identify which method matches the description from Step 3. Option a, Dideoxy Chain Termination method, is the correct one.

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Key Concepts

These are the key concepts you need to understand to accurately answer the question.

Fred Sanger
Fred Sanger was a British biochemist who made significant contributions to the field of genetics and biochemistry. He is one of the few scientists to have been awarded the Nobel Prize in Chemistry twice.
Sanger's first Nobel Prize was awarded in 1958 for his work on the structure of proteins, particularly insulin.
However, his second Nobel Prize in 1980 was for his development of the DNA sequencing technique, which revolutionized the field of genomics.
His approach to DNA sequencing is often referred to as the Sanger method.
Dideoxy Chain Termination method
The Dideoxy Chain Termination method, also known as the Sanger sequencing method, is a technique used to determine the nucleotide sequence of DNA.
This method involves synthesizing new DNA strands based on a single-stranded template. The process uses a primer that binds to the DNA template and a DNA polymerase enzyme to synthesize the complementary strand.
A crucial aspect of this method is the incorporation of dideoxynucleotides, which cause the termination of DNA synthesis when they are added to the growing DNA strand.
Due to the lack of a 3'-OH group, dideoxynucleotides prevent any further nucleotides from being added, effectively halting DNA synthesis at specific points.
The resulting DNA fragments of varying lengths are then analyzed to determine the sequence of the original DNA template.
Dideoxynucleotides
Dideoxynucleotides (often abbreviated as ddNTPs) are modified nucleotides used in the Sanger sequencing method.
Unlike regular deoxynucleotides (dNTPs), dideoxynucleotides lack the 3'-hydroxyl (3'-OH) group on the sugar molecule.
This missing 3'-OH group prevents the formation of a phosphodiester bond with the next nucleotide, thus terminating DNA chain elongation.
In Sanger sequencing, four types of dideoxynucleotides are used, each labeled with a different fluorescent dye corresponding to one of the four DNA bases: adenine (A), cytosine (C), guanine (G), and thymine (T).
When incorporated into the growing DNA strand, the fluorescent dyes provide a way to identify the end nucleotide of each fragment, allowing the sequence to be read after separation by electrophoresis.
This method of using ddNTPs to terminate DNA synthesis was a pivotal innovation in the development of more advanced DNA sequencing techniques.

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Most popular questions from this chapter

Which of the following is not one of the proteins involved during the formation of the replication fork? a. helicase b. ligase c. origin of replication d. single-strand binding proteins

A mutation has occurred in the DNA and in the mRNA for a gene. Discuss which would have a more significant effect on gene expression. Why? a. Both will result in the production of defective proteins. The DNA mutation, if not corrected, is permanent, while the mRNA mutation will only affect proteins made from that mRNA strand. Production of defective protein ceases when the mRNA strand deteriorates. b. Both will result in the production of defective proteins. The DNA mutation, if not corrected, is permanent, while the mRNA mutation will not affect proteins made from that mRNA strand. Production of defective protein continues when the mRNA strand deteriorates. c. Only DNA will result in the production of defective proteins. The DNA mutation, if not corrected, is permanent. Production of defective protein ceases when the DNA strand deteriorates. d. Only mRNA will result in the production of defective proteins. The mRNA mutation will only affect proteins made from that mRNA strand. Production of defective protein ceases when the mRNA strand deteriorates.

Prior to the work of Hershey and Chase, scientists thought that inheritance involved 鈥渘ucleoproteins.鈥 The amount of information to be transmitted between generations did not seem consistent with the chemical simplicity of the few nucleotides found in polymers of deoxyribonucleic acids in comparison to the diversity of protein polymers. Briefly explain: 鈥 the relationship between the structure of polymeric DNA and the information stored 鈥 the relationship between the interactions between base pairs on complementary strands of the double helix and Chargaff鈥檚 observation on the relative abundance of nucleotides in DNA 鈥 the meaning of the statement from the Nature publication on the structure of DNA by Watson and Crick: 鈥淚t has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material.鈥

Explain why patients with Xeroderma Pigmentosa are more prone to cancer than the rest of the population a. Xeroderma Pigmentosa patients cannot employ the nucleotide excision repair mechanism. When these patients are exposed to UV light, thymine dimers are formed and they are not able to repair this defect. These dimers distort the structure of DNA and cause them to have a high risk of contracting skin cancer. b. Xeroderma Pigmentosa patients can employ the nucleotide excision repair mechanism. When these patients are exposed to UV light, the thymine dimers are formed and they are able to repair this defect. These dimers do not distort the structure of DNA and they have moderate risk of contracting skin cancer. c. Xeroderma Pigmentosa patients cannot employ the nucleotide excision repair mechanism. When these patients are exposed to UV light, the adjacent adenine forms dimers and they are not able to repair this defect. These dimers distort the structure of DNA and they have high risk of contracting skin cancer. d. Xeroderma Pigmentosa patients cannot employ the nucleotide excision repair mechanism. When these patients are exposed to UV light, the adjacent thymine cannot form thymine dimers and they are not able to repair this defect. The non-formation of dimers distorts the structure of DNA and they have high risk of contracting skin cancer.

What is the initial mechanism for repairing nucleotide errors in DNA? a. DNA polymerase proofreading b. mismatch repair c. nucleotide excision repair d. thymine dimers

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