Hemophilia

Hemophilia is a Sex-Linked bleeding disorder that slows blood clotting. It can cause people to bleed more often from little injuries and bleed alot longer from things such as surgery, any injury, or having a tooth pulled. Hemophilia can cause severe internal bleeding into joints, muscles, organs, or the brain. It can cause massive swelling and even death.

Hemophilia A is caused my a change in the F8 gene and Hemophilia B is caused by a mutation in the F9 gene. A is the classic one while B is known as christmas disease. A form of B is known as hemophilia B Leyden and that causes excessive bleeding in adulthood but gets better after puberty. Hemophila C is the rarest and takes much longer to clot.

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The symptoms are simply bleeding. They may not be noticed until later in life during surgery or after trauma. Diagnostics and Detection are normally after a severe bleeding episode.

People can be treated by receiving the clotting factor by intravenous infusions which is through a vein.

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Hemophilia is more common in men. 1 in 400 to 1 in 5000 males are born with Hemophilia A and 1 in 20,000 are born with Hemophilia B worldwide. it affects all ethnic groups.

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Life expectancy isnt really affected but some may bleed to death and internal bleeding may cause problems.

Scribe- Sammy K

Today In Class we first talked over electrophoresis, plasmids and also Restriction Sights.

- Gel Electrophoresis is used to separate DNA fragments.

- Shorter fragments move faster and more farther away from the starting point compared to the longer fragments.

- Gel Electrophoresis is used often in crime scenes because it compares the DNA from the crime scene to a certain prospect.

Plasmid: is a small circular DNA which is located in the cytoplasm of a bacteria.

(Here is a picture of Plasmid DNA formation)

This picture shows how bacteria can be transformed using recombinant plasmids.

Restriction Sight: It is the location where the restriction enzyme can be cut at.

Recombinant DNA molecules are made up of DNA from a various group of sources. The restriction enzymes cut the DNA at certain spots (Restriction Sight), and then produces "sticky ends". When two DNA molecules are cut with the same restriction enzyme, then the sticky ends will bond together (in the fragment) of the DNA which have sides which are complementary.

HW:
RESPOND TO MUDDIEST POINTS BY TOMORROW.

PUNNETT SQUARE RE-TAKES TOMORROW

Muddiest Point

My muddiest point is the sticky ends. When the circle gets cut does anything get taken out of it, or does the section of DNA only get added?

Stem cell help

I need help with stem cells. Are there multiple types of stem cells? Also do they have any purpose at all in the body?

Muddiest Point

my muddiest point is how are stem cells transformed in to specified cells

JoeM's Muddiest Point

My muddiest point is probably the blood typing. I'm confused as to how each type is made such as Ia and Ib make AB. And is ii the only way you can have O as your blood type?

CRI-DU-CHAT SYNDROME- OJ

Cri du chat syndrome, also known as chromosome 5p deletion syndrome, Lejeune’s syndrome is a Genetic DISORDER.It is called cri du chat because at birth newborns cry sounds like a cats cry. it is caused from formation of egg or sperm by unequal recombination during meiosis. The Genetic Disorder was first identified in 1963 by Geneticist Jerome Lejeune(who also discovered down syndrome). Cri du chat is caused by Deletion of the top part of Chromosome 5 (shown BELOW)

Many genes are missing from the deletion and some may contribute to to the symptoms of the disorders. the life expectancy is normal.Here are the Symptoms

• small at birth
• respiratory problems
• Larynx doesn't develop properly which cause the cat like cry 
• have a small head 
• wide eyes small bridge of the nose 
• Have trouble walking and talking 
• Poor muscle tone, skeletal problems, hearing and sight problems 
• Severe Mental Retardation 
• Behavior problems

the disorder is identified byt infants cry like a cat, Microcephaly, Poor muscle tone,  mental retardation, test  in the mothers womb. There are no treatment for Cri du chat  but they can go to therapy to improve language skills and develop normally as possible.

Muddiest Point

My muddiest point is stem cells. I dont get what they are and where they come from.

Marfan Syndrome

The Marfan Syndrome is a defect in your gene that makes the fibrillin 1 an important protein for connection tissue. This defect takes place in the chromosome 15. There are many ways to identify a person with Marfans Syndrome. Everyone who is effected with this has at least three features in different parts of the body. Many symptoms are...

1. Long legs
2. Long arms
3. Curved spine (hunch back)
4. Long, thin fingers
5. Near sighted
6. Stretch marks on skin

There is no easy way to tell if you have this syndrome, there is no easy bloo

d test you have to be evaluated by a doctor. There is no cure but there is therapies that can limit complications. The way you would get these treatments is by seeing specialized doctors that would make an individualized program. The life expectancy for a person with this disease is just a little bit under the normal life expectancy. This disorder is pretty uncommon one in every six thousand babies is born with Marfan. And there is no difference in babies born with Marfin in different ethnicities.

Muddiest Point

My muddiest point is when you are doing pedigrees, is it always contain X and/or Y to show male or female or is it always just dominant and recessive letters, example B-brown b-blonde? Or can it be either or depending on the question?

Muddiest Point

my muddiest points are the meaning of autosomal and sex-linked. I know that they are opposites (autosomal is the opposite of sex- linked), but what do they really mean?

Wolf-Hirschhorn Syndrome

Wolf Hirschhorn affects 1 in 50,000 new born babies. Wolf Hirschhorn is caused by the partial deletion of the short arm on chrmosome 4. (pictured below)

Wolf Hirschhorn is characterized as a person with a disappearance on one of the arms of chromosome 4. Physical features include: Intrauterine growth restriction, mental retardation, characteristic facial dysmorphism, microcephaly, earlobe anomalies and closure defects ( cleft lip, coloboma of the eye, and cardiac septal affects ). Wolf-Hirschhorn also causes the person to have seizures and to have dental defects such as missing teeth. However 85-90% of cases of Wolf- Hirschhorn Syndrome are not inherited they are simply caused during a mutation when the egg and sperm meet. However the disorder may be inherited by a parent with the same disorder. The life expectancy for someone with Wolf-Hirschhorn is about 25. The oldest person still living with Wolf-Hirschhorn syndrome was born in 1949. Currently no population is a risk for Wolf-Hirschhorn syndrome because it is so rare. To date there are no known treatments for Wolf-Hirschhorn Syndrome.

AndyD's Muddiest Point

My muddiest point is the difference between autosomal recessive and autosomal dominant and how they work.

Scribe for 12/13

Today we started off the class with discussing the homework that was due today well Lucky for you Unit packet pages 73-74 got moved to tomorrow so go over them at home so your prepared to talk about them tomorrow. Then we reviewed the Karyotyping Web Quest in which you're gonna have to know:

1. How to see a disorder by only looking at the karyotype.
2. Determine what that disorder is.
3. Also to determine what chromosome it's on and how it effects that chromosome

Here are two examples of a Disorder:

Turner Syndrome

1. Only one X chromosome on woman
2. On karyotype you can see that there is only one X chromosome

Down Syndrome

1. Has one extra copy of chromosome 21
2. On Karyotype look for three chromosomes on 21

Then we started taking notes on Genetic Engineering is when you practically copy and paste genes. You Manipulate DNA into ways that are useful to you. We also learned About PCR or Polymerase Chain Reaction is when you use Polymerase to make more DNA. We then learned about Restriction Enzymes and those are enzymes that precisly cut and recognize a certain base sequence. We then finished off class with a nice movie on how Forensics use DNA to capture suspects.

Muddiest Point

My muddiest point is how do you know if a problem is a certain type of autosomal or if it is a sex linked problem.

Muddiest Point

My muddiest points are what happens in each step of meiosis.

Muddiest Point

Can you please explain to me how cells can be transformed?

Muddiest Point

Can you please explain to me how cells can be transformed?

My Muddiest Point

My muddiest point in this unit was the differences between prophase 1 and prophase 2 of the two phases of meiosis. How are they different?

Hemochromatosis

        Hemochromatosis is a disorder which causes the body to absorb too much iron from the person's diet. Hemochromatosis is an autosomal recessive disorder, which means that the person can only inherit the disorder if they inherit the abnormal (recessive) gene from both parents. There are two genetic mutations associated with hemochromatosis; C282Y and H63D. The numbers 282 and 63 label the place of the defects of the HFE gene located on chromosome number 6.
        People with hemochromatosis have no symptoms at a young age and have no idea that they have the disorder. Symptoms may not appear until the person is in their forties or fifties. Iron deposits in the skin cause the skin to become darker and look slightly orange. There is also an elevated level of iron in the blood. Iron deposits in the pancreas result in a decrease of the production of insulin causing diabetes mellitus. Iron deposits in the heart muscle can cause heart failure and abnormal rhythms of the heart. Iron deposits in the liver can cause scarring of the liver and an increased risk of liver cancer.
        Most people with hemochromatosis are diagnosed at an early age and show no symptoms. The disorder us detected when elevated levels of iron in the blood are found in blood testing.
        The most common and most effective treatment for hemochromatosis reduces the level of iron in the body. This treatment is called phlebotomy and in this treatment blood is withdrawn from the veins in the person's arm. Usually, the person goes in every one or two weeks to withdraw one unit of blood, which has 250 mg of iron in it. Chelation therapy uses chemical compounds and proteins from the body to remove toxic metal molecules from the blood. Also, a diet with lots of vitamin C can help absorb some of the iron in the blood. Fruits and vegetables are good for the diet and too much red meat should be avoided.
        Type 1 hemochromatosis is one of the most common genetic disorders in the United States, affecting about one million people. It mostly affects people of Northern European descent. All other types of hemochromatosis is very rare; only a small number of people are affected with hemochromatosis (not type 1) worldwide.
        Most people affected with hemochromatosis life the average life expectancy.

                                                                           

Iron is contained in red blood cells.

Loeys-Dietz Syndrome

Loeys-Dietz Syndrome also known as LSD is a autosomal dominant syndrome which is caused by a mutation in the genes encoding for transforming growth factor. It is inherited from the persons parents and since it is autosomal dominant only one parent needs to have the syndrome to pass it on. To diagnos LSD Doctors will check the patients family history, a physical exam, and do a genetic test to see if they have lsd.

Some of the symptoms of Loeys-dietz are,

1. Split uvula
2. Defects in heart and brain
3. Weak bones
4. skin changes
5. Defects of the spine and chest
6. far apart eyes (picture to right)

Depending on how sever The persons LSD is there are different types of treatment. If they have a split uvula doctors can usually perfom sugery to fix this. For far apart eyes, doctors cant do much for it and for weak bones it will be sugested not to play high impact sports. LSD is a relativly new disease and there is no pevelence in society known. Depending on the severity of LSD and treatment quality The life expectance is any were from 20-70 years old.

Muddiest Point

My muddiest point is the difference between autosomal recessive and autosomal dominant what is the difference. How do they work.

Phenylketonuria

Phenylketonuria, also known as PKU is a disease that affects the way your body breaks down proteins. PKU is an autosomal recessive inherited disease, so you inherit one infected chromosome from your mom and one infected chromosome from your dad. If you were looking at the karyotype of someone with this disease, you would notice that there is a mutation in a gene on chromosome 12. This mutation is a protein gene mutation that codes for protein PAH. If someone does not have enough PAH, phenylalanine builds up in their blood, which leads to poisoning their nerve cells. When babies are first born, they show no signs. If they continue living without being treated, they can get severe brain damage, such as Epilepsy. This can also give them behavioral problems and stunt their growth. Other signs can be eczema, musty body odor, small head and fair skin. When babies are first born they are tested for this disease. A small blood sample is take from their heel or arm and the doctors test it for the level of phenylalanine. If there is a high level of phenylalanine, then the baby has the disease. If you have the disease you need to eat a protein-free diet because many proteins contain phenylalanine. Infants are given a special formula that does not contain phenylalanine. As you get older with this disease, you need to avoid protein rich foods, such as meats, cheeses, nuts and eggs. On average one out of every fifteen thousand babies are born with this disease. If you follow the specific diets of this disease the life expectancy is the same as if you lived regularly.

Huntington's disease

Huntington's Disease is a disorder in which the nerve cells in certain brain parts are wasted. HD is inherited by parents. Huntington's Disease is a genetic defect that take place on chromosome 4. There are no known treatments yet for HD. The main goal is to slow down the symptoms. People with HD usually die within 15-20 years. The HD itself is a reason people die, but another common reason is suicide. There are 2 forms of HD. The more common one develops at the age of mid 30's and 40's. The more rare type develops at a young age. If the parents have HD there is a 50% chance that the child will also have it.

Symptoms

• Behavioral disturbances

• Hallucinations

• Irritability

• Moodiness

• Restlessness or fidgeting

• Paranoia

• Psychosis

  
  

  
  

Maple Syrup Urine Disease

Maple syrup urine disease is a disorder that is passed down genetically. People with this disease cannot break down some proteins, resulting in urine that smells like maple syrup. This disease is caused by a gene defect, in which the amino acids leucine, isoleucine, and valine cannot be broken down. The affect of not being able to break the amino acids down is a buildup of these chemicals in the blood. If this disease is untreated, it can lead to seizures, comas, and death. Maple syrup is not very common, only affecting about 1 in every 185,000. The genes related to this disease are mutations in the BCKDHA, BCKDHB, DBT, and DLDD genes. These genes provide instructions for making proteins for breaking down the certain amino acids. This disease is AUTOSOMAL RECESSIVE, so people can be a carrier of the disease, but show no symptoms. If not treated, this disease is very deadly, so for a treatment, a special diet is needed to follow. This diet may be a protein free diet, or avoiding eating foods with the amino acids leucine, isoleucine, and valine.

Sickle Cell Disease

Sickle cell disease is inherited by both the parents passing a defective copy of the Gene. If one parent passes it down while the other dose not that child is a carrier. Less oxygen can travel to the organs of the person who has this disease causing the organs to die. Red blood cells of the people with the disease live less than normal red blood cells so people have a low anemia. Sickle cells get stuck and cause pain to the affected person. People who have this live 30 years less than normal people. Most states routinely check newborns for the disease but if not there is a test called hemoglobin electrophoresis which you can take to see if you are affected or carrier. Most people with this take a dose of penicillin a day and folic acid. People who have this also get blood transplants to get healthy blood cells. This disease mostly affects African Americans in America. 1 out of every 500 African Americans in america are affected.

Patau's Syndrome

Patau's syndrome also known as trisomy 13 happens when there are 3 copies of genetic material from chromosome 13.
This syndrome occurs when extra DNA in trisomy 13 appears in body cells. The extra chromosome interfers with body development and other development.

The symptoms:

• Cleft lip of palate



• Clenched hands



• Extra fingers or toes



• Seizures



• Skeletal abnormalities (limbs)



• Scalp Defects (missing skin)



• Small Eyes



• Small head



• Small Lower jaw

There can be signs of congenital heart disease like for example the heart being on the right side of the chest instead of the left

The problems with is syndrome is that people get this syndrome at newborn stage. The complications are that it may cause deafness, heart failure, feeding problems, trouble breathing, and visions problems.

Spinal Muscular Atrophy

Spinal Muscular Atrophy is an autosomal recessive genetic disorder that is inherited by having both parents carriers of the gene. The chances of the child of two carriers is 25% or 1 out of 4. Someone who has Spinal Muscular Atrophy have either a missing or mutated SM1 gene. This gene produces a protein called Survival Motor Neuron. Motor neurons are nerve cells in the spinal cord which send out nerve fibers to muscles throughout the body. Because this protein is necessary for survival, without it, nerve cells will stink and die over time and this causes muscle weakness. As children with SMA grow, their bodies become weak, fragile and stressed.

SMA can be diagnosed through a blood test, specifically looking for the presence or absence of the SM1 gene. Doctors may also request a muscle biopsy.

Currently there are no drugs to treat Spinal Muscular Atrophy but there has been over $17million invested into SMA drug development.

Muddiest Point 11/5

My muddiest point are the haploid and diploid. I don't really understand what they are.

Nuerofibromatosis

Neurofibromatosis or NF1 is the growth of noncancerous tumors that form underneath the skin. This disorder is caused by a mutation on chromosome number 17. This disorder is Autosomal Dominant and if one parent has the mutation then half the children will have NF1. When people get this dicease they develop Neurofibrons which are tumors that can block arteries and can cause a stroke or heart attack. Each persons symptoms vary because the genes are so different that the severity of the symptoms vary.

Doctors have not found a cure for NF1 but tumors can be surgically removed and corect malformed bones. In very few cases the tumors actually become cancerous which is then treated with chemotherapy. The wierd thing about NF1 is that they may only have a couple of tumors or they may have thousands.

Blooms Syndrome

Blooms syndrome is an inherited birth disorder. People diagnosed with Blooms syndrome are very short and weigh very little when they are born. On average, they only reach about 5 ft at the tallest when they are adults. Blooms syndrome causes the affected to have a very different and uncommon face. They typically have a long narrow face, a larger nose, and a high pitched voice. Men that have Blooms syndrome are unable to produce sperm. The disorder is most common in central and eastern Europe. One third of the affected are Ashkenazi Jews.

The condition is inherited by the auotosomal recessive pattern. The parents that produce a baby with this disorder are typically both carriers of the recessive/mutated gene. But, this does not mean that the parents have the disorder, they are carriers, not the affected.

Many with this syndrome are more prone to being diagnosed with cancer and diabetes. Many have severe troubles with learning. They also have many infections to the ears, respiratory tract, and lungs during their infancy.

Sister chromatid exchange: left is normal and right is Blooms syndrome.

Canavan Disorder

Canavan disorder is inherited if both parents are carriers of the defective gene. Both of the parents need to be carriers in order to have an affected child. If both parents carry the gene mutation, there is a 25% chance for the pregnancy to have a child that will be affected with the disease. Canavan disorder is a degenerative disease in the brain. It is also located on chromosome 17.

Symptoms of Canavan disorder usually appear in the first 3 to 6 months of childhood and increase rapidly. Symptoms include lack of motor development, trouble with feeding, abnormal muscle tone (stiffness or weakness), and an abnormally large, poorly controlled head. Blindness, hearing loss, and paralysis may also occur.

Canavan disease can be identified with a blood test before the birth of the baby. The blood test can screen for missing enzymes or mutations in the gene. Canavan disorder causes progressive brain atrophy. There is no cure for this disease or a standard course of treatment.

Although this disorder can occur in any ethnic group, it is mostly common throughout Ashkenazi Jews. Studies show that this disorder affects 1 in 6,4oo to 13,500 people in the Ashkenazi Jewish population.

The life expectancy with Canavan disorder varies. Many affected individuals only survive through childhood. Only some may survive into their teen years or beyond.

This is a picture of a boy who has been affected with Canavan disorder.

Muddiest Point- PatrykS

My muddiest point is the autosomal recessive and autosomal dominant, how does that all work?

Muddiest Point 11/5

One of my muddiest points is the difference haploid and diploid. I am confused with the 2N and N stuff. Another muddiest point are the pedigrees. I don't really know how to read them or decide the genotypes, or whatever you have to do them. Is there an easier way to understand them?

Wilson Disease-Patryk Swietek

Wilson Disease

Wilson disease is a genetic disorder that doesn't let your body get rid of extra copper. Copper is required for your body but having too much of it is poisonous. To get Wilson disease, you need to inherit two not normal copies of ATP7B gene from each parent. To carry the disease, you only need one. The symptoms of this disease are attacks at the liver, the nervous system or both. This results in swelling of the liver, fluid buildup and being bruised more easily. Good news is that Wilson disease can be diagnosed with physical examination and laboratory tests. It can also be treated although it requires lifelong treatment to control copper amount in body. People who get the disorder detected early get good treatment, can have good health.

ATP7B GENE

The ATP7B gene is pointed out in the image above. This gene is located on the long arm of chromosome 13.

Cystic Fibrosis- Sammy Kim

Cystic Fibrosis

Cystic Fibrosis is inherited when chromosome 7 (called CFTR) contains a defective gene. If both parents which contain Cystic Fibrosis or are carriers of the disease pass the flawed gene onto their child, then the child will be affected with Cystic Fibrosis. If the child only inherited one of the flawed gene, then the child will be called a carrier which is not affected with the disease, but it can possibly be passed down and affected on their children. When people is affected with this disease, they have symptoms such as: coughing, a salty-tasting skin, weight loss, and a lot more. They also have thick mucous clogs in the airways for the lungs which rises the chance of having an infection. This happens because the protein produced by this gene helps salt move in and out of the cells, but without it the lungs will be clogged up with thick and sticky mucous. People with Cystic Fibrosis can be detected by the excessive amount of salt in their sweat and also by taking a sample of their blood. There is no cure for this genetic disorder, but there are a few treatments which makes the people with the disease live longer. The treatments for it are repeatedly hitting the back to free up the mucous in the chest, inhaled antibiotics which keep the airways open and resist the infection in the lungs, and gene therapy (When a healthy chromosome 7 is placed into the lung cells of the person with the disease to fix the defective gene). Cystic Fibrosis is most common with the white people population in the United States. It is said that it is found in 2,500 to 3,500 White newborns in one year. There are about 30,000 people in the United States which is affected by Cystic Fibrosis. The average life expectancy for someone with Cystic Fibrosis is around 30 years old.

(HERE IS A PICTURE OF A CHROMOSOME 7 WHICH CONTAINS A DEFECTIVE GENE).

Beta Thalassemia

Beta Thalassemia is a blood disorder. It reduces the amount of hemoglobin you produce, which is a protein that contains iron. Hemoglobin in red blood cells is what carries oxygen to cells throughout your body.

Beta Thalassemia is caused by mutations on the HBB gene which can be found on the short arm of chromosome 11. HBB is a gene that holds instructions for making the protein beta-globin, which is a component in hemoglobin. It is inherited from an autosomal recessive pattern. You can inherit this disorder from your parents even though they don't show symptoms and signs from the condition.

Beta Thalassemia is classified into two types depending on how severe your symptoms are. There is Thalassemia intermedia and the most severe is Thalassemia Major. Those with thalassemia major will experience symptoms or signs of this disorder in the first two years of their lives. Children with thalassemia major will experience delayed puberty, yellowing of the skin and eyes, not being able to gain weight, enlarged liver, spleen, and heart, and their bones maybe misshaped. Those with thalassemia major may experience such severe symptoms that they may need to frequently get blood tranfusions to restore their red blood cell supply. Those with thalassemia intermedia usually only experience anemia. Anemia is a condition in which your body doesn't have enough healthy red blood cells.

You're diagnosed with beta thalassemia depending on how severe your anemia is and by taking a blood test to check for any red blood cell or hemoglobin abnormalities. If your results come back abnormal for either, genetic testing for mutations on the HBB gene will be taken.

Treatment that is available for thalassemia major is having regular transfuctions to help increase the production of iron and correct anemia. The only existing cure is to have a bone marrow transplant from either an identical sibling or a donor. For thalassemia intermedia, treatment consists of having frequent therapy that involves having red blood cell tranfusions.

This is a common blood disorder worldwide. The chances of inheriting this disorder is 1 in 3,600 individuals. It occurs most often in people from North Africa, the Middle East, Central and Southeast Asia, India, and Mediterranean countries.

The life expectancy for someone that isn't treated will die in their early 30's and those that are treated can live a normal lifespan.

GabbyM's Muddiest Point

My muddiest point for this chapter is what kind of errors can happen during meiosis.

Paul s muddiest point

My muddiest point of unit 5B is the difference between trisomys and monosomys and how they create a genetic disorder/syndrome.

Thanks,
Paul S

Fragile X

Fragile X syndrome is caused by changes in a part of the x chromosone, and is an inherited intellectual disability. This has both mental and physical symptoms.
-Flat feet, flexible joints, large body size, large forhead, long face, and soft skin.
There are very few ways to detect the syndrome other then Large head circumference in babies, Mental retardation, and Large testicles after the start of puberty. There is no treatment for fragile X. Males are usually effected more by the disease then females. Fragile X syndrome occurs 1 in 4,000 males, and 1 in 8,000 females. This syndrome does not effect the life expectancy of males or females.

Paul Salay

AndyD Scribe Class 12-6-11

Today in class we learned about Genetic Disorders!

We started out by BrooklynC stamping our homework stamp-sheet and then discussing the homework with our groups of 3. After everything was settled at the beginning of class we went over the homework as a class and went over the problems that were unclear to us. After the class discussion we took some notes on Probability, What autosomal was, and what sex linked was. Probability was one of the things we discussed as we went over our Pedigree homework. We discussed the chances of having male and female babies and babies with disorders.

We also made the probability ratio of males and females in our class and their siblings

(pictured below). Males on bottom females on top because for some reason the image turned out awkward.

Homework

• Up 51-52
• Read Chapter 14.2 in textbook.
• Quiz on Thursday on the Punnet Square w/ co-dominance and etc.

Next Scribe will be- MichaelM

Andy D Scribe Post 12-5-11.

Today in class we learned about PEDIGREES!

In class we first started out by discussing our homework with our new seating chart and groups that Mrs. Stein arranged for us. After our discussion with our peers we went over the correct answers as a class and discussed any of the questions that were kind of weirdly worded and tricky. After going through the answers we got into more detail with Blood typing and sex linked problems, especially the hybrid blood types.

Please ignore the names mentioned in the Pedigree above..... However the main lesson of today was Pedigrees. What are Pedigrees? They a chart made up of family members from one generation continuing on till the current. Pedigrees are used to trace disease or a specific trait within a family. Males in the chart are shown as Squares, and Females are shown as circles. However people that are shaded in have that trait or disease the is being tracked, women however with a half shaded circle are carriers of the disease or trait and may pass it on to one of their children and so on.

HOMEWORK!

• UP 47-50
• Read Chapter 14.1 in the textbook ( no duh where else?)
• Quiz on how to solve all of the punnet squares and problems on how to find a genotype and phenotype ( codominance etc.), Pedigrees will also be on the quiz!

Late Scribe, finally letting me post!

In class on 11/29/11, we got new seats! We took a small quiz on meiosis, which we got to look over with our new seat partners. We then took a closer look at meiosis and mitosis using a double bubble map, which was the homework due for the day. Meiosis is the production of gametes, which are haploid cells (cells with 23 chromosomes instead of the typical 46.) We discussed meiosis for the rest of the class with five minutes to spare to work on the homework, which is UP 29-31 and to read 11.1 and 11.2.

Next scribe will be Joey M!

Class on 11/30-12/1

11/30

In class today we went over our homework which was trying out the punnet squares. After we went through the homework, we partnered up and did an activity where we flipped a coin to determine the phenotypes of each item. We then drew the baby according to the traits we got. The only homework was to finish the questions that went with the baby lab.

12/1

Today in class we turned in our baby labs. After that we took a self check quiz on vocabulary and using punnet squares. We then learned about Incomplete Dominant traits which are traits that have twodominant genes with both being expressed. We then learned how to use dihybrid punnet squares.(Look down for more) Our homework is to do pages UP 33-38 and read 11.3!

http://www.youtube.com/watch?v=cvTt-azvHsA

ANDY is the Next Scribe

11/28

In class on 11-28-11. We started a NEW UNIT!! The new unit we are starting is about Meiosis, Genetics, and Genetic Technology. The way we started the new unit out was to compare and contrast Meiosis to Mitosis or review the phases of Meiosis (this was homework over thanksgiving break).

Today in class we took notes on Meiosis. Mrs. Stein asked us a question she said What is the goal of Meiosis? The goal of Meiosis is making the egg and sperm cell.

There are 23 pairs of homologous cells. In total there are 46. Each pair comes from your parents. Cells with a double set of chromosome are diploid (2n). Cells with one set of chromosomes are haploid (n). In Meiosis the chromosomes are haploiod. A haploid has half the number of chromosomes.

Where does Meiosis occur? Meiosis occurs in the ovary and testes.



Our body cells are diploid cells (2N) 2N=46 N=23


Gametes are sex cells and they are haploid. The fertilization restores the diploid state (N+N=2N).
Zygote is a fertilized egg (2N).

This is a picture of Meiosis I and Meiosis II.
In Meiosis I there is Prophase I, Metaphase I, Anaphase I and Telophase I. Then in Meiosis II the cells is formed a clevlege. The end result is Cytoskinesis and 4 cells are created. In this picture there is 2 cell divisions-Meiosis I and II.

The homework for today 11-28-11 was to read 11.4 with double bubble map or flow map (your choice).
Unit Packet 13-14-READ/COLOR/ANOTATE.

Next scribe is JessicaB :).

How DNA was discovered!

Heres a 20 minute video about how James Watson discovered DNA! Told from the man himself!

http://www.ted.com/talks/james_watson_on_how_he_discovered_dna.html

Thanks to Jack G for reminding me!

Friday, 11/18

In class on Friday, we did a lab regarding protein synthesis. The point of the lab was to understand the roles of mRNA(messenger RNA) and tRNA(translation RNA) in protein synthesis. To help our understanding, we constructed a model of protein synthesis. FIrst, we built two stands of DNA. Then we separated the two stands and built the corresponding strand of mRNA (using uracil instead of thymine). After that, we separated the mRNA strands form the DNA strands and made a codon of the mRNA strand, or the tRNA strand. Then we attached an amino acid to the right tRNA molecule by it's R-group. DNA polymerase is the enzyme needed for DNA replication. The enzyme used to build mRNA and tRNA is RNA polymerase.

The two steps in protein synthesis are transcription and translation. Transcription takes place in the nucleus and forms mRNA strands from one of the strands of DNA. Translation occurs in the cytoplasm on a ribosome and the codons of mRNA (tRNA) are translated into amino acids to form proteins.

Our homework for this weekend was to finish UP 23-28, UP 39-40 (online), UP 15-20, read section 13.3, and finish our tribune article, all due on Monday.

Don't forget to study for the unit test this Tuesday! 


Next scribe will be Elizabeth.

EXTRA CREDIT!

Alright guys... 2 extra credit opportunities!

Click on this link and answer the following questions.

1. What color is the RNA backbone in this activity?

2. What 3 amino acids make up the polypeptide chain at the end of the protein synthesis activity?

First 4 people to email me the answers will get extra credit!

Opportunity #2... click on this link, enter in your FULL name... and complete the 'quiz'. You will get extra credit based on your score. This opportunity will expire on Sunday at midnight!

11/16

Today in class we went over our homework from last night which was the Double Bubble Map for DNA vs. RNA.

Then for the rest of the period we went over protein synthesis. We took notes on this during class and Mrs. Stein put up the notes on Moodle. We only took notes on the first two slides in the powerpoint. If you are a person that likes having organized notes, then read through the rest of the slides in the powerpoint. These are the two slides we took notes on:

There are two parts to protein synthesis: transcription and translation. Mrs. Stein had us draw this picture. It represents the whole process of protein synthesis. As you can see transcription happens in the nucleus and translation happens in the cytoplasm on a ribosome.

Here is a picture that represents what happens in the translation process more clearly. In translation, mRNA attaches to a ribosome. A tRNA carries only ONE amino acid. In the picture, the cloves shape is the tRNA and the little circle that it is holding represents the amino acid. The anticodon on the tRNA matches with the codon on the mRNA. Once the tRna has finished, it LEAVES the ribosome. All the amino acids join into a long chain called a polypeptide. This long polypeptide is what makes PROTEIN. Remember: Amino acids MAKE UP protein.

HOMEWORK: 1) 13.1 & 13.2 Flow Map of Protein Synthesis is due TOMORROW! If you need help use Moodle because Mrs. Stein put up some animations that are very helpful.


2) Tribune Article due Monday 11/21


3) There will be a test on Tuesday 11/22 on everything that we have covered in this chapter. Use your objectives to help you study!


The next scribe will be Andrijana.

Class 9/15

Today at the beginning of class we handed in UP 7-14. Then, we had a reading check on the reading from last night, which was 12.3. After the reading check we took some notes. Below are the notes we took today.

DNA & CHROMOSOMES: LARGEST- Chromosome (46)

Gene: segment of DNA which codes for protein.

Double Helix

SMALLEST- nucleotides (sugar-dexoyribose, phosphate, nitrogen bases)

DNA REPLICATION:

~During S-phase of interphase

-2 copies needed for mitosis

~Each strand serves as a template for the new strand

~produces 2 identical DNA molecules

~semi-conservative replication: each new molecule contains one old strand and one new

Here are some links to help with these notes:

http://www.fed.cuhk.edu.hk/~biology/teaching/genetics/animations/transcription.htm

http://www.susanahalpine.com/anim/Grolier_Anims/DNA.htm

Homework:

1. Read 13.1-Double Bubble Map: DNA vs. RNA- due tomorrow (11/16)

2. Read 13.1 and 13.2- Flow Map: "Protein Synthesis"- due Thursday

3. Tribune Article- due Monday

4. Unit Test- Tuesday

The next scribe will be GABBY

Class 9/15

Scribe 11/14

At the start of class today our UP pages 7 and 8 were checked. They will be turned in tomorrow along with pages 9-14. Tonight you will also read 12.3 in the textbook. Due on monday is the Tribune article and tuesday will be our unit test.

Today in class we did a lab that can be found on UP pages 13 and 14. We were instructed to create a strand of DNA based on the code it gave us for the left strand. When we completed the 9 rung ladder of DNA it should look like this:

Then you were to duplicate the DNA strand and should come out with two identical DNA ladders.

Sribe for 11/10/11

Even though the class period was about 40 minutes long, we covered a lot of stuff in class.

HOMEWORK:
-Read and Understand UP 11-14 (lab)

-UP 7-8

-Make magazine article or tribune (Due: 11/21)

CLASS ACTIVITY:

We went to our lab groups to discuss the following terms: DNA, Protein, Gene, Nitrogen Base, Phosphate, Nucichleotide, Structure. We took this words and explained them by writing up a paragraph to define all of them. All the groups presented their paragraph in class and were judged by mrs. Stein on how well they were defined in the paragraph. Then when comparing everyones performance, she found the word gene, as she expected to be the one that everyone didn't do so well on. This brings us to the question:

What the definition of a Gene?

INCORRECT ANSWER: "things that make up who we are"
CORRECT: Segment (unit) of DNA which codes for proteins...these proteins determine our traits.

CLASS NOTES:

DNA- deoxribonucleic acid

SLIDES

DNA STRUCTURE AND COMPONENTS

*Double Helix- 2 strands form a twisted ladder
*Subunits of nucleotides contain:
- Sugar
- Phosphate group
- Nitrogen group
*Backbone ("uprights") made of deoxyribose and phosphate

NITROGEN BASES

*Purines- 2 rings
- Adenine
- Guanine
*Pyrimidines- 1 ring
-Thymine
-Cytosine
*Order of the bases contains the "code"to make proteins

scribe for 11/8!

Today in class, we discussed our last disease of the day. The disease was lyme disease. The agent of this disease is bacteria. The vector of this disease is the mosquito. Then, for the rest of class we reviewed for the TEST TOMORROW. We went over the quiz we took yesterday, and watched a

few short clips to review. The review session for our disease and immunity test will be

tomorrow morning, so make sure you try to make it of you have any questions!

Also, don't forget to check out the muddiest points, and make sure you've posted your comments!

STUDY STUDY STUDY! Check the moodle page to review with animations that Mrs. Stein

has posted! Good luck tomorrow!