Part 1: Genetics – From Genes to Proteins, Mutations (Chapter 10)?

Monday, June 13th, 2011 at 5:36 am  
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A question from Tigerlily2682: Part 1: Genetics – From Genes to Proteins, Mutations (Chapter 10)?
Overview: Genetic information in DNA is transcribed to RNA and then translated into the amino acid sequence of a Protein.

A) Step 1 – Transcription: During the process of transcription, the information in the DNA codons of a gene is transcribed into RNA.

Suppose that gene X has the DNA base sequence 3’-TACCCTTTAGTAGCCACT-5’.

Question: What would be the base sequence of RNA after transcription occurs? Turn this in.

(In this particular example, assume that the RNA product does not require processing to become mRNA. In other words, the transcribed RNA becomes the mRNA sequence.)

B) Step 2 – Translation: During protein synthesis at the ribosome, the base sequence of the mRNA codons is translated to the amino acid sequence of a protein.

Question: Using the mRNA that you transcribed above, use the genetic code table to determine the resulting amino acid sequence? Turn this in.

And, turn in the answer to these questions:

What is the significance of the first and last codons? What meaning do these codons have for protein synthesis?

C) Mutations: A mutation is defined as a change in the base sequence of DNA. This may occur as a “mistake” in DNA replication, for example.

Suppose that during DNA replication, two mutant DNA sequences are produced as shown below.

For the 2 mutated DNA sequences, you will investigate how these changes might affect the sequence of amino acids in a protein.

Question: For each of the two, you will need to first transcribe the mRNA, and then use the genetic code table to determine the amino acid sequence.

Turn these in, and state whether the protein sequence changes for each.

Question: Then, explain why a change in amino acid sequence might affect protein function. Turn in your answer.

Here is the original sequence, followed by two mutated sequences, 1 and 2:

Original sequence 3′- TACCCTTTAGTAGCCACT-5’

Mutated sequence 1) 3’-TACGCTTTAGTAGCCATT-5′

Mutated sequence 2) 3’-TAACCTTTACTAGGCACT-5’.

Part 2: Inheritance of Traits or Genetic Disorders (Chapter 12)

Bob and Sally recently married. Upon deciding to plan a family, both Sally and Bob find out that they are both heterozygous for cystic fibrosis, but neither of them has symptoms of the disorder.

Set up and complete a Punnett Square for cystic fibrosis for this couple; turn in the Punnett square.

When doing the Punnett Square, C = normal allele; and c = allele for cystic fibrosis.

Note: You can use the Table function in MS Word to create and fill in a Punnett Square.

Questions:

Based on the Punnett square, calculate chances (percentages) for having a healthy child (not a carrier), a child that is a carrier for the cystic fibrosis trait, and a child with cystic fibrosis? Turn in these percentages.

Part 3: Cell division, sexual reproduction and genetic variability (Chapter 11)

Eukaryotic cells can divide by mitosis or meiosis. In humans, mitosis produces new cells for growth and repair; meiosis produces sex cells (gametes) called sperm and eggs.

Although mutations are the ultimate source of genetic variability, both meiosis and sexual reproduction also can contribute to new genetic combinations in offspring.

Question: How do both meiosis and sexual reproduction (fertilization) produce offspring that differ genetically from the parents? Be sure to talk about steps in meiosis that increase variability as well as the process of fertilization.

Most detailed answer:

Answer by Kendi Rosenberg
part one:
A) AUGGGAAAUCAUCGGUGA
B) AUG(the start code/ methoninie), GGA (Glycine), AAU (Asparagine), CAU (Histidine), CGG (Arginine), UGA (Stop code)

The significance of the fist and last codons are that theay are the start code and the stop code.

The meaning they have for protien synthesis is that the start code tells where to start synthesis and the stop code tells where to stop synthesis.

C) Mutated sequence 1) AUGCGAAAUCAUCGGUAA
AUG (start code/ methonine), CGA (Arginine), AAU (Asparagine), CAU (Histidine), CGG (Arginine), UAA (Stop code)

Mutated sequence 2) AUU GGA AAU GAU CCG UGA
AUU (Lisoleucine), GGA (Glycine), AAU (Asparagine), GAU (Aspartic acid), CCG (Proline), UGA (Stop code)

The Change in Amino Acid sequence might effect the protien function because for example in mutated sequence number 2 there is no start code meaning this would never get translated.

Part 2:

Here i drew a punnet square for you and took a picture of it… here is the link

I drew this for you

They have a 25% chance of having a child that is not a carrier.
They have a 50% chance having a child who is a carrier.
They have a 25% chance of having a child has cystic fibrosis
1:2:1 – genotypic
3:1- phenotypic

Part 3:

Meiosis and sexual reproduction contribute to genetic variation by independant assortment- random distribution of homologus churomosomes. Also by crossing over and random fertalization.

How about adding your own answer to the comments below!

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What Are the Chances I Am a Cystic Fibrosis Carrier?

Monday, June 14th, 2010 at 7:01 pm  
Comments (2)
arrowheadadventure asked:

I tested negative for the 23 most common mutations of the gene that causes CF. I know that there is a 4% chance for caucasians like myself to be a carrier, but would assume that is less for me due to my test results. My wife is a CF carrier and we have a 1 year old daughter. She still worries that our daughter is at risk.

Technorati Tags: Caucasians, Cystic Fibrosis, Mutations

Fight Cystic Fibrosis With Vitamins and Over the Counter Products

Wednesday, February 17th, 2010 at 5:03 am  
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Cystic fibrosis is a hereditary disease that affects the entire body, causing progressive disability and early death. Cystic fibrosis affects the entire body and impacts growth, breathing, digestion, and reproduction. Difficulty breathing and insufficient enzyme production in the pancreas are the most common symptoms.

The Pancreas of patients with Cystic Fibrosis fails to produce enough enzymes that are necessary to break down food. As a result the food eaten retains its fats and most of its nutrients as it passes through the body.

The bronchial tubes in the lungs also malfunction and produce a thick, sticky mucus. Germs multiply in this mucus and cause respiratory infection such as pneumonia, accompanied by a cough and high fever that is more severe than normal.

A multitude of other symptoms, including sinus infections, poor growth, diarrhea, and potential infertility (mostly in males) result from the effects of cystic fibrosis on other parts of the body. Patients with Cystic Fibrosis also sweat profusely and their perspirations also contains an unusually high percentage of salt.

Cystic fibrosis is the most common life-limiting recessive disease among people of European heritage. Two copies of the recessive mutated gene, one from each parent is needed by the human body to develop Cystic Fibrosis.

Because cystic fibrosis testing is expensive, testing is often performed on just one parent initially. If that parent is found to be a carrier of a CFTR gene mutation, the other parent is then tested to calculate the risk that their children will have cystic fibrosis. Cystic fibrosis can result from more than a thousand different mutations and, as of 2006, it is not possible to test for each one. Most commercially available tests look for 32 or fewer different mutations.

Couples who are at high risk for having a child with cystic fibrosis; i.e. cystic fibrosis has developed in family members, will often opt to perform further testing before or during pregnancy. After birth cystic fibrosis may be diagnosed in newborn with sweat testing, or genetic testing.

Most states and countries do not screen for cystic fibrosis routinely at birth. Children with cystic fibrosis typically do not gain weight or height at the same rate as their peers and occasionally are not diagnosed until investigation is initiated for poor growth. Males tend to have a longer life expectancy than females but the reason is unknown.

Use a mask nebulizer and other inhalations treatments are the most common forms of treatments for cystic fibrosis. The goal is the treating and limiting the amount of lung damage caused by thick mucus and infection. Albuterol and ipratropium bromide are inhaled to increase the size of the small airways by relaxing the surrounding muscles. As lung disease worsens, breathing support from machines may become necessary.

Most individuals with cystic fibrosis take additional amounts of vitamins A, D, E, and K and eat high calorie meals.

Common Vitamins and over the counter products can help with treating Cystic Fibrosis such as Vitamin E, Vitamin K, Vitamin A, Lactase Enzyme, Papaya, Protein Tablets, Vitamin B, Amino Acid and L-Carnitine.

Dr. Harry Schwachman reported “most patients with cystic fibrosis have low levels of vitamin E”. Vitamin E protects lung tissue form inhaled pollutants and aids the functioning of the immune system.

Vitamin K helps the blood to clot after and injury.

A number of studies have suggested that taking antioxidants such a Vitamin A reduces the risk of bronchoconstriction. Vitamin A is stored in the liver and fat cells of the human body and can reach toxic levels. DO NOT take more than the recommended dosage of Vitamin A.

Lactase Enzyme makes milk products more readily digestible.

Papaya contains lipase, which assists in Fat and Cellulose digestion.

Protein tablets increase protein intake.

All of the different Vitamin Bs taken together as B-Complex work together as a team to perform vital biological processes, such as energy production and efficient metabolic function. Vitamin B boost energy levels and help fight fatigue.

Amino Acid help regulate growth, digestion and maintaining the body’s immune system.

L-Carnitine is essential for the body’s ability to turn food into energy. L-Carnation increases energy at the cell level by increased fat burning, increases the body’s ability to remove toxic disease-causing compounds and helps cells live longer.

Always consult your doctor before using this information.

This Article is nutritional in nature and not to be construed as medical advice.

By: David Cowley

About the Author:

David Cowley has created over 50 articles about the relationship between diseases and vitamins. For other Articles on Diseases and Vitamin Needs feel free to visit my Web Site at http://www.dfcinvestment-team.com

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