Once again, Khan Academy is here to make life easier! This is a nice lecture introducing you to heredity, which is basically what we learned this chapter. It starts at the beginning with the basics, like physical traits, and goes into homozygous and heterozygous as the video goes in. The video goes into dominant and recessive traits, and also touches on the different types of dominance there are, i.e. codominance. The video uses proper terminology like allele, homozygous, heterozygous, dominant, recessive, etc. The video also goes into Punnett Squares.
Ok so here's another nice video! Basically, the guy has a pedigree and is trying to figure out what type of disease is present in the family. He takes you step by step in eliminating choices and deducing what kind of disease is present in the family. Instead of looking at the pedigree as one big thing to figure out the disease, he goes step by step through the generations, which is different from what many people do. Being as though DWebs has asked questions using pedigrees, it would make sense for us to see this on the exam, so this would be a great help! Wait, you're probably gonna read this after the exam... Oh well...
Tuesday, February 21, 2012
Good Golly Guys Got the Gene!
I just love alliterations... Don't you? I know my amazing title just blew your mind so I'll give you some time to settle down... You alright now? Let's go!
Alright so you may be wondering exactly what gene is this girl talking about. Well, get ready for this... As this article explains, scientists have finally identified the gene the Gregor Mendel used to manipulate in his pea plants experiments! As you should recall, these are the experiments that Mendel used to establish the basic laws of genetics!
Scientists have specifically pinpointed the gene he used to control the pea plants color. This gene is common to many plant species, and the plants use it to break down a green pigment molecule. This is now the third of seven genes Mendel manipulated that researches have identified! Before, researchers were never able to identify the gene for seed color because the pea genome was so huge. Luckily, plant geneticist Ian Armstead of the Institute of Grassland and Environmental Research in Aberystwyth, Wales, and the lead author of a report on the findings was able to stumble upon the gene.
Armstead and his colleagues were working to locate the sequence of a gene called staygreen (sgr) in the meadow grass Festuca pratensis. Some variants of this gene cause the plant to remain green even in unfavorable conditions like drought, because they cannot break down a green pigment. Festuca is genetically similar to rice, which has already had its genome sequenced. Armstead and his group compared genetic markers on the sgr region of the grass's chromosome to the respective region in the rice genome. They found 30 potential genes, including one similar to other pigment-metabolizing proteins. They then tested and confirmed that this was the equivalent to the sgr gene. To then find out if the equivalent sgr pea gene was one of the genes Mendel manipulated in his experiments, the researchers picked out the location of its sequence from pea plants that had different seed colors. Lo and behold, it was found on the same part of the chromosome as the gene that Mendel used!
Alright so you may be wondering exactly what gene is this girl talking about. Well, get ready for this... As this article explains, scientists have finally identified the gene the Gregor Mendel used to manipulate in his pea plants experiments! As you should recall, these are the experiments that Mendel used to establish the basic laws of genetics!
Scientists have specifically pinpointed the gene he used to control the pea plants color. This gene is common to many plant species, and the plants use it to break down a green pigment molecule. This is now the third of seven genes Mendel manipulated that researches have identified! Before, researchers were never able to identify the gene for seed color because the pea genome was so huge. Luckily, plant geneticist Ian Armstead of the Institute of Grassland and Environmental Research in Aberystwyth, Wales, and the lead author of a report on the findings was able to stumble upon the gene.
Armstead and his colleagues were working to locate the sequence of a gene called staygreen (sgr) in the meadow grass Festuca pratensis. Some variants of this gene cause the plant to remain green even in unfavorable conditions like drought, because they cannot break down a green pigment. Festuca is genetically similar to rice, which has already had its genome sequenced. Armstead and his group compared genetic markers on the sgr region of the grass's chromosome to the respective region in the rice genome. They found 30 potential genes, including one similar to other pigment-metabolizing proteins. They then tested and confirmed that this was the equivalent to the sgr gene. To then find out if the equivalent sgr pea gene was one of the genes Mendel manipulated in his experiments, the researchers picked out the location of its sequence from pea plants that had different seed colors. Lo and behold, it was found on the same part of the chromosome as the gene that Mendel used!
Japanese Flounder Sex Determination
Perhaps you'll get a clever title next time...
SO in humans, the sex of an individual basically is determined by whether or not they have XX or XY. Females are XX and males XY. This is not the case in all animals, as we saw in this chapter. As this article explains, Japanese Flounder also use the XX/XY system to determine the sex of their species. However, unlike humans the fish can be induced to become phenotypic males or females. This is done by gender rearing them in either 18 or 27 degrees Celsius.
This suggests that exposure to high temperature causes cyp26b1 mRNA expression and delays meiotic initiation of germ cells. It does do by elevating cortisol levels during gonadal sex differentiation in Japanese flounder.
SO in humans, the sex of an individual basically is determined by whether or not they have XX or XY. Females are XX and males XY. This is not the case in all animals, as we saw in this chapter. As this article explains, Japanese Flounder also use the XX/XY system to determine the sex of their species. However, unlike humans the fish can be induced to become phenotypic males or females. This is done by gender rearing them in either 18 or 27 degrees Celsius.
Because of this, Japanese flounder are great to use to study the molecular mechanisms that cause temperature-dependent sex determination. Researchers previously showed that cortisol causes female-to-male sex reversal by directly suppressing mRNA expression of ovary-type aromatase (cyp19a1). cyp19a1 is a steroidogenic enzyme that converts androgens to estrogens in the gonads.
An inhibitor of cortisol prevented XX flounder from becoming masculine at 27 degrees. This suggests that masculinization by high temperature is because of the suppression of cyp19a1 mRNA expression caused by elevated cortisol levels during differentiation in the gonads. In this current study, researchers found that exposure to high temperatures during gonadal sex differentiation upregulates mRNA expression of retinoid-degrading enzyme (cyp26b1). This happens concurrently with the masculinization of XX gonads and also delays meiotic initiation of germ cells. Cortisol induces cyp26b1 mRNA expression thereby suppressing specific meiotic marker synaptonemal complex protein 3 (sycp3) mRNA expressions in gonads during the sexual differentiation.This suggests that exposure to high temperature causes cyp26b1 mRNA expression and delays meiotic initiation of germ cells. It does do by elevating cortisol levels during gonadal sex differentiation in Japanese flounder.
Tuesday, February 14, 2012
Chapter 15 Helpful Hints!
Once again Khan Academy comes to the rescue. Even though we've been learning about meiosis for years now, I am always confused when it comes to diploid and haploid and that "n" thingy. So this video was super helpful because it help explain in nice terms as Khan Academy tend s to do. The video is a nice lecture that one could watch before an exam for a nice refresher. Of course it uses all of the terms we know and explains meiosis 1 and meiosis 2. It also compares and contrasts meiosis to mitosis every now and again, which I think is very helpful because I have a feeling there's going to be a question or two about comparing and contrasting the two processes on an exam.
This is a nice quick video on the cell cycle. Although it is brief, it has a decent amount of details and information packed into it. For example, structures like centromeres and kinetochores are identified and labeled when they are in action during the cell cycle. The video also explains the G1, S, and G2 phases during interphase which many people and many videos tend to forget is part of the cell cycle.
This is a nice quick video on the cell cycle. Although it is brief, it has a decent amount of details and information packed into it. For example, structures like centromeres and kinetochores are identified and labeled when they are in action during the cell cycle. The video also explains the G1, S, and G2 phases during interphase which many people and many videos tend to forget is part of the cell cycle.
Silly Cilia!
Awww you're taken aback by my super cute title?? How sweet, how sweet. Give yourself some time to calm down. You ready? Off we go!
As I am hoping you already know, mitosis is the process of cell division that produces two identical daughter cells. So this article talks about the role of cilia proteins during mitosis. Researchers at the University of Massachusetts Medical School have discovered a role for the cilia proteins IFT88, that was previously unknown. Oh hey look, since most of us are aiming to go to medical school, if you go there you can tell them you already know things about them! Lucky you. You're welcome. Anyway, so yes, they discovered a previous unknown role for IFT88. This newly discovered roles suggests that this could be a possible alternative or contributory cause for cilia-related diseases like primary ciliary dyskinesia, and polycystic kidney disease. Here's a nice picture of some actual cilia.
IFT88 is part of a family of transport proteins and cellular machinery that is in charge of moving materials from the cell body to the cilia. It is a slender protrusion responsible for motility and sensory input known for its ability to build cilia. If IFT88 is not present, cilia are either not able to form or defective. Scientists have linked cilia dysfunction to a number of ciliopathies. IFT88 absence has been linked to polycistic kidney disease (PKD), which is characterized by the presence of multiple cysts in the kidneys. PKD is also believed to be caused by cilia dysfunction in kidney cells.
Stephen J. Doxsey, PhD, professor of molecular medicine and biochemistry & molecular pharmacology and cell biology and lead author of the study, and his colleagues observed that the IFT88 protein is present at the poles of the mitotic spindle. They knew 1FT88 and other proteins were present at the spindle poles, but their functions were unknown. Benedicte Delaval, PhD, found that IFT88 plays a part in transporting materials required for building the spindle poles during cell division. Ergo, the loss of IFT88 protein during mitosis causes there to be a delay in mitotic division and misalignment of the direction and plane of cell division. This of course is not good.
Both cilia and spindle fibers arise from centrosomes, leading Doxsey to hypothesize that there is a deeper, underlying connection between the two. Until more research and test and studies are conducted... the world may never know...
As I am hoping you already know, mitosis is the process of cell division that produces two identical daughter cells. So this article talks about the role of cilia proteins during mitosis. Researchers at the University of Massachusetts Medical School have discovered a role for the cilia proteins IFT88, that was previously unknown. Oh hey look, since most of us are aiming to go to medical school, if you go there you can tell them you already know things about them! Lucky you. You're welcome. Anyway, so yes, they discovered a previous unknown role for IFT88. This newly discovered roles suggests that this could be a possible alternative or contributory cause for cilia-related diseases like primary ciliary dyskinesia, and polycystic kidney disease. Here's a nice picture of some actual cilia.
IFT88 is part of a family of transport proteins and cellular machinery that is in charge of moving materials from the cell body to the cilia. It is a slender protrusion responsible for motility and sensory input known for its ability to build cilia. If IFT88 is not present, cilia are either not able to form or defective. Scientists have linked cilia dysfunction to a number of ciliopathies. IFT88 absence has been linked to polycistic kidney disease (PKD), which is characterized by the presence of multiple cysts in the kidneys. PKD is also believed to be caused by cilia dysfunction in kidney cells.
Stephen J. Doxsey, PhD, professor of molecular medicine and biochemistry & molecular pharmacology and cell biology and lead author of the study, and his colleagues observed that the IFT88 protein is present at the poles of the mitotic spindle. They knew 1FT88 and other proteins were present at the spindle poles, but their functions were unknown. Benedicte Delaval, PhD, found that IFT88 plays a part in transporting materials required for building the spindle poles during cell division. Ergo, the loss of IFT88 protein during mitosis causes there to be a delay in mitotic division and misalignment of the direction and plane of cell division. This of course is not good.
Both cilia and spindle fibers arise from centrosomes, leading Doxsey to hypothesize that there is a deeper, underlying connection between the two. Until more research and test and studies are conducted... the world may never know...
Super Amazingly Cool Spindle Assembly Checkpoint (SAC SAC!!)
Hey pretty person! If you are a boy then... take that as you will. I know you're in awe from my fetch title I'll give you a second to calm down. Are you good? Ok, let us begin!
So this article talks about the Spindle Assembly Checkpoint (SAC) and its importance in the cell. So as I'm sure you know meiosis is the process used by germ cells to produce gametes. If you didn't know that then... woe is you. Anyhoo, meiosis consists of meiosis 1 and meiosis 2. Meiosis 1 separates homologous chromosomes and meiosis 2 separates sister chromatids. Here's a picture, as they always make things better.
Now to separate or pull the chromosomes into daughter cells, the cell produces spindle fibers. If the spindle fibers connect to the centromeres of the chromosomes they are called kinetochore spindle fibers, and they are called non-kinetochore spindle fibers if they do not connect to the spindle fibers. If chromosomes are not separated properly, it leads to daughter cells being anupleoid, which will lead to the cell being killed once fertilization has occurred or birth defects in the offspring. Here's a picture showing spindle fibers although I'm hoping you already know what they look like...
In mitosis, SAC exists to ensure that proper chromosome segregation has occurred. In the last decade, most notably in the past several years, researchers have found a checkpoint similar to SAC in meiosis! There is evidence that points to the existence of SAC functions in meiosis. This evidence is provided by studies on many components of SAC. This includes but is not limited to SAC proteins mitotic-arrest deficient-1 (Mad1), Mad2, budding uninhibited by benzimidazole-1 (Bub1), Bub3, BubR1 and Mps1. I was going to be lazy and not list all of them but alas, I shall list them all as it's probably the right thing to do. More componenets include microtubule-kinetochore attachment regulators Ndc80 complex, chromosomal passenger complex, mitotic centromere-associated kinesin (MCAK), kinetochore null 1 (KNL1) and Mis12 complex and spindle stability regulators. So in conclusion, SAC does exist in meiosis but in order to fully understand it and all of its components, more research needs to be done.
So this article talks about the Spindle Assembly Checkpoint (SAC) and its importance in the cell. So as I'm sure you know meiosis is the process used by germ cells to produce gametes. If you didn't know that then... woe is you. Anyhoo, meiosis consists of meiosis 1 and meiosis 2. Meiosis 1 separates homologous chromosomes and meiosis 2 separates sister chromatids. Here's a picture, as they always make things better.
In mitosis, SAC exists to ensure that proper chromosome segregation has occurred. In the last decade, most notably in the past several years, researchers have found a checkpoint similar to SAC in meiosis! There is evidence that points to the existence of SAC functions in meiosis. This evidence is provided by studies on many components of SAC. This includes but is not limited to SAC proteins mitotic-arrest deficient-1 (Mad1), Mad2, budding uninhibited by benzimidazole-1 (Bub1), Bub3, BubR1 and Mps1. I was going to be lazy and not list all of them but alas, I shall list them all as it's probably the right thing to do. More componenets include microtubule-kinetochore attachment regulators Ndc80 complex, chromosomal passenger complex, mitotic centromere-associated kinesin (MCAK), kinetochore null 1 (KNL1) and Mis12 complex and spindle stability regulators. So in conclusion, SAC does exist in meiosis but in order to fully understand it and all of its components, more research needs to be done.
Thursday, February 9, 2012
Chapter 14 Helpful Hints!
Okey dokey here we go!
This video was great! It explains point mutations, insertions, and deletions in a clear and informative manner. It also seems like it would help before a Dr. Weber exam because it explains the effects of mutations on organisms as well, and we all know how DWebs likes to ask questions like that.. The video explains the difference between mutations that occur during mitosis along with meiosis. I also really liked this video because along with explaining the mutations, it showed videos of how the mutations occur and also how the body tries to fix the mutations. Enjoy!
Ok so this is a pretty cool video. Rather than explaining the cell cycle which we have honestly studied to death and then some... this video focuses on and explains the Cell Cycle Checkpoints. For example, in class we learned about cyclin and CDK, but the video goes into more detail about how those molecules work. It also talks about p53 and it's functions like stimulating the production of proteins that bind and inactivate CDK molecules, activating enzymes required to repair DNA, and apoptosis. Again, I like this video because it goes into what happens when some of these molecules lose their functions because we all know how a certain Bio teacher enjoys putting questions like these on the exams... Well, enjoy!
This video was great! It explains point mutations, insertions, and deletions in a clear and informative manner. It also seems like it would help before a Dr. Weber exam because it explains the effects of mutations on organisms as well, and we all know how DWebs likes to ask questions like that.. The video explains the difference between mutations that occur during mitosis along with meiosis. I also really liked this video because along with explaining the mutations, it showed videos of how the mutations occur and also how the body tries to fix the mutations. Enjoy!
Ok so this is a pretty cool video. Rather than explaining the cell cycle which we have honestly studied to death and then some... this video focuses on and explains the Cell Cycle Checkpoints. For example, in class we learned about cyclin and CDK, but the video goes into more detail about how those molecules work. It also talks about p53 and it's functions like stimulating the production of proteins that bind and inactivate CDK molecules, activating enzymes required to repair DNA, and apoptosis. Again, I like this video because it goes into what happens when some of these molecules lose their functions because we all know how a certain Bio teacher enjoys putting questions like these on the exams... Well, enjoy!
Mutation Makes Mirror Movements
Alright heroes/cool kids, this article talks about a specific mutation and the effect it has on the body. There is a mutation that messes with your immune system causing you to always do mirror movements. Meaning if you raise your right hand, the left one is going up with it. In more formal terms, one side of the body always involuntarily mirrors movements done voluntarily on the other side of the body.
Now you may be thinking that this must be such an annoying disease to live with but people like Andree Marion live with it every hour of every day. Marion is a 47-year-old accountant from St. Sauveur, Quebec and it turns out her 19-year-old son also has mirror movements. In fact if you trace Marion's family back four generations, of her 23 blood relatives, about half of them have mirror movements. These rare mirror movements are caused by a gene defect.
A neurologist and geneticist at the University of Montreal named Guy Roleau was the senior author of a study that uncovered the mutation found in Marion and her relatives. The wires of the nervous system cross. Axons from motor neurons in the brain sweep over the middle of the body before connecting to other motor neurons in the spinal cord. These motor neurons then connect to the muscles. Roleau comments on how scientists still don't know why or how this happens in humans.
Mirror movements are quite rare and are normally found only in people with disorders of nervous system crossings. No one in Marion's family had any such disorder so Roleau and colleagues were given a great opportunity to see just how wiring went wrong. What they found was the in Marion and relatives, the right side of the brain controlled the right hand... but also the left hand. Some axons crossed over, but some did not. The axons that didn't cross over would just go on the exact same spinal motor neuron, just on the opposite side of the spinal cord.
Since Marion and many relatives had mirror movements, Roleau and his team knew it was hereditary. While it took them one and half year to collect the DNA from all of the relatives it only took them 3 months to find the faulty gene. the faulty gene was deleted in colorectal cancer (DCC). This mutation interferes with DCC's interaction with netrin, which is a diffusible extracellular protein that helps guide axons across the body's midline while the body is developing. DCC is expressed in the midline of the nervous system. Once axons sense the protein they begin to move towards it. However, this mutation cuts the level of functionality of the protein in Marion and relatives. In essence, they don't have enough of the protein to get all of the nerves to cross over.
Marion explained that she always noticed the mirror movements since she was a child, but they were never a big concern because she was able to do what she wanted. Marion can type and drive without any difficulty. She joked the only thing she has a problem with is playing pool. What a jokester Ms. Marion is... She also said she has to be careful when cutting and cooking food. Marion also noted that her mirror movements are more pronounced than her sons. For her son, the mirror movements are more in his hands, while hers are also in the biceps and toes.
Now you may be thinking that this must be such an annoying disease to live with but people like Andree Marion live with it every hour of every day. Marion is a 47-year-old accountant from St. Sauveur, Quebec and it turns out her 19-year-old son also has mirror movements. In fact if you trace Marion's family back four generations, of her 23 blood relatives, about half of them have mirror movements. These rare mirror movements are caused by a gene defect.
Mirror movements are quite rare and are normally found only in people with disorders of nervous system crossings. No one in Marion's family had any such disorder so Roleau and colleagues were given a great opportunity to see just how wiring went wrong. What they found was the in Marion and relatives, the right side of the brain controlled the right hand... but also the left hand. Some axons crossed over, but some did not. The axons that didn't cross over would just go on the exact same spinal motor neuron, just on the opposite side of the spinal cord.
Since Marion and many relatives had mirror movements, Roleau and his team knew it was hereditary. While it took them one and half year to collect the DNA from all of the relatives it only took them 3 months to find the faulty gene. the faulty gene was deleted in colorectal cancer (DCC). This mutation interferes with DCC's interaction with netrin, which is a diffusible extracellular protein that helps guide axons across the body's midline while the body is developing. DCC is expressed in the midline of the nervous system. Once axons sense the protein they begin to move towards it. However, this mutation cuts the level of functionality of the protein in Marion and relatives. In essence, they don't have enough of the protein to get all of the nerves to cross over.
Marion explained that she always noticed the mirror movements since she was a child, but they were never a big concern because she was able to do what she wanted. Marion can type and drive without any difficulty. She joked the only thing she has a problem with is playing pool. What a jokester Ms. Marion is... She also said she has to be careful when cutting and cooking food. Marion also noted that her mirror movements are more pronounced than her sons. For her son, the mirror movements are more in his hands, while hers are also in the biceps and toes.
Anthracycline and Cancer
So this article talks about anthracyclines and the role they play in treating many childhood cancers. Anthracyclines are a class of drugs used in cancer chemotherapy derived from Streptomyces bacteria. Although anthracyclinescan help to get rid of the cancer, they are quite harmful to the heart. The effects on the heart can be seen while treatment is going on or even many years after treatment has ended. Before deciding to use anthracyclinesone, one should be familiar with its antitumor effects and cardiotoxic effects.
To see what would be better, scientists conducted a series of tests in order to be able to compare antitumour efficacy of treatment including or not including anthracyclines in children with several different childhood cancers. Researchers discovered that at the moment evidence is not strong enough to say that anthracyclines have an increased antitumour effect in acute lymphoblastic leukaemia (ALL) as compared to treatment without anthracyclines. However, there's some suggestion saying that anthracyclins do have an increased antitumor effect. In order to make a definite conclusion on anthracyclin effect on ALL, more research and tests need to be done. Researchers only found limited data on Wilms' tumour, habdomyosarcoma/undifferentiated sarcoma, Ewing's sarcoma, non‐Hodgkin lymphoma, and heptoblastoma, so they could not draw any conclusions. This is a relatively new concept, so at the moment there is no data for other childhood cancers. Although a general link between anthracyclins and childhood cancers has been shown, more high quality research needs to be done before definite conclusions can be drawn.
Subscribe to:
Posts (Atom)