Chapter 16: Useful Materials

When I found this video I thought it was the cutest thing ever! So I thought I would share it with you. Basically, this video talks about how genes carry down traits through family members. It gives several example of different types of traits, such as gender and blood type. The video also talks about how some traits are inherited from just one parent, while others are a mixture of both parents. Most traits are influenced by not just one but many genes, which combine with one another to form a single trait... isn't that neat?! Anyways, I think you should watch this video because it is just too cute!

This animation (CLICK HERE) shows an example of a Punnett square. What is a Punnett square, you ask? Well a Punnett square is a diagram that is used to predict an outcome of a particular cross or breeding experiment. What I like about this animation is that it gives several example of how to use a Punnett square. It also makes you decide what the genotype and phenotype of the Punnett square is. This animation was quite helpful and if you ever need help in understanding how a Punnett square works, I advise you to check out this animation!

Spo11 Catalyzing Meiosis-Specific DNA!

From reading the title, you might be just as confused as I was when I first read this article. But not to fear! Your confusion will hopefully be cleared up by the end of this post (cross your fingers!). Now on to the important stuff...the abstract of this article is from PubMed talks about Spo11, which is a protein involved in double-strand breaks (DSBs). DSB initiates meiotic recombination in S. cerevisiae, a species of yeast that is used in numerous biological studies.

Lets pause for a second and ponder what meiotic recombination might mean...done pondering? Well meiotic recombination is a genetic recombination process by which a molecule of nucleic acid (usually DNA, but can also be RNA) is broken and then joined to a different one. Meiotic recombination in eukaryotes facilitates chromosomal crossover. The crossover process leads to offspring's having different combinations of genes from those of their parents, and can occasionally produce new chimeric alleles (artificially constructed gene).

Spo11 is one of several proteins required for DSB formation, and was identified when DSB, in certain mutants, would covalently attach to it. Spo11 is strongly involved in these findings as "the catalytic subunit of the meiotic DNA cleavage activity." Why is this important? Well because these findings are the "first identification of a biochemical function for any of the gene products involved in DSB formation." Therefore, not only are these findings important, but they also have clear, supporting evidence that the mechanism of meiotic recombination initiation is evolutionarily preserved.

Article:

Meiosis-specific DNA double-strand breaks are catalyzed by Spo11, a member of a widely conserved protein family.

A New Discovery in Mitosis??? (drumroll...)

I am guessing that you all want to know what the new discovery is right? Well there is no discovery.....................haha just kidding; I fooled you for a second didn't I? Well researchers from The George Washington University Medical Center, have discovered something that could possibly "revolutionize the way scientists think about key aspects of cellular lifecycle." It can also offer new opportunities for cancer researchers to help reduce the progression of cancer. This new discovery can shed some light into the understanding of mitotic cell division.

What is mitotic cell division, you may ask? Well mitosis is the process by which a eukaryotic cell separates the chromosomes in its cell nucleus into two identical sets, resulting in the production of two daughter cells from a single parent cell. According to Rakesh Kumar, Ph.D., chair of the GW Department of Biochemistry and Molecular Biology, "this represents a crucial moment when the division of genetic material is still equally distributed. An even exchange is critical for stable genetic changes." Therefore, if something were to go wrong during cell division, such as chromosomal mutations (deletions, duplications, inversions, and translocations), it could lead to an unequal production of abnormal cells and quite possibly result in cancer.

Researchers from the GW Department of Biochemistry and Molecular Biology may have discovered a missing link about the protein, Arpc 1b, which acts as an activator as well as a substrate for Aurora A, "an enzyme which plays a central role in cellular reproduction in normal cells but is over-expressed in several cancers." The missing link found is the role that Arpc 1b plays in beginning the cell cycle and how the process is kept in balance.

Not only is this finding beneficial in keeping the cell cycle in harmony, it may also offer a potential target for pharmaceutical therapy. You might be asking, how can this happen? Well researchers discovered that Arpc1b promotes tumorigenic properties of breast cancer cells when it is over-expressed. With this new discovery, researchers hope to uncover a way to suppress Arpc 1b activity in cancer cells, in order to have this important biological event kept in pristine balance.

Article:

Missing Link in Cell Mitosis Discovered: The Role of Protein in Controlling Cell Division Unveiled

Chapter 15: Useful Materials

When I first found this video, I knew that I just had to post it! This video describes the phases of mitosis through the song, "I Got a Feeling" by the Black Eyed Peas. The song explains all the phase of mitosis (interphase, prophase, metaphase, anaphase, telophase, and cytokinesis) and what happens during each phase. I think it is a catchy tune and it is just too cute! Seriously, words cannot describe it's cuteness (haha yup, thats right, I'm calling a song cute...deal with it). Anyways, I recommend that you should listen to this awesome song because you just might learn a little something about mitosis.

What the Fudge Are Tumor Supressor Genes???

Although the abstract for this article is super short, I shall attempt to expand this paragraph as much as possible. The abstract does not explain much; but it does talk about the mutation of tumor suppressor genes and tumor suppressor proteins. For those of you reading this post that are pulling your hair out and screaming, "what the fudge are tumor suppressor genes" at your computer screen, allow me to take you out of your misery. Tumor suppressor genes, when normal, encodes a protein that helps prevent cancerous growth. However if tumor suppressor genes are mutated, their normal function is eliminated and cancer may occur.

The main thing that the abstract explains for tumor suppressor gene mutation is that the mutation is "thought to contribute to tumor growth by inactivating proteins that normally act to limit cell proliferation." For example, a tumor suppressor gene is like the brake pedal on a car. It normally keeps the cell from dividing too quickly, just as a brake keeps a car from going too fast. When something goes wrong with the gene, such as a mutation, cell division can get out of control.

There are several tumor suppressor proteins, but only two of them (p53 and pRb) are understood thoroughly enough in detail. Both of these proteins have a common role in the events of transcription and phosphorylation that are required for a cell to pass from the G1 to S phase.

(The image above is the cell cycle with the checkpoint proteins: cyclin and cyclin-dependent protein kinases (cdks))

Lets start with p53, (or protein 53) which is responsible for proteins that can either repair damaged cells, or cause damaged cells to die, a process called apoptosis. When the gene is not working due to a mutation, these proteins that repair cells or eliminate damaged cells are not produced, and abnormal cells are allowed to divide and grow. A mutation in the p53 gene (located on chromosome 17) is the most common mutation found in cancer cells, and is present in over 50% of cancers.

Now lets think about pRb, (or retinoblastoma protein) which functions to prevent excessive cell growth by inhibiting cell cycle progression until a cell is ready to divide. pRb is part of a category of tumor suppressor genes that encodes proteins that are negative regulators or inhibitors of cell division. The Rb protein negatively controls a regulatory transcription factor called E2F that activates genes required for cell cycle progression from G1 ro S phase. The binding of Rb proteina and E2F inhibits its activity and prevents cell division.

Hopefully that thoroughly explained tumor suppressor genes and its functions. If you are still unsure about the role of tumor suppressor genes, think of my analogy I said earlier in this post. A tumor suppressor gene is like a brake pedal: tumor suppressor gene regulates cell division just like how a brake pedal regulates the speed of a car! (Hehe I probs can guess what you are thinking..."Serina why are you just so clever?")

Article:

Tumor suppressor genes

Gene Mutation: Beneficial or Detrimental?

Did you read the title of this post? Well you should have, if not go read it now (do it...you won't)! Anyways, from reading the title, you might be asking yourself: how can gene mutation can be beneficial? Usually when people think of mutations, they relate it to being harmful to the body because gene mutations are changes in the DNA structure that can alter a particular gene.

Well this article gives an example of how gene mutation can be somewhat helpful. In Berlin, a baby was born with bulging thighs and biceps that were credited to a unique beneficial genetic event. Now you could be asking yourself: how is this mutation beneficial? According to the article, the mutation was advantageous in the short run because the child able to lift seven-pound dumbbells with arms extended. I am not sure how scientists seem to think that this ability is beneficial to the child. Is he going to enter a weight lifting competition? Although this capability may seem profitable now, the child's future is still a mystery. Dr. McNally states that, "the boy is still very young and that problems could occur later in his life."

It was discovered that the child had a mutation in the gene that produces a protein called myostatin. And me, being the clueless airhead that I am, did not know what myostatin was... good job Serina! So I googled the word (thank god for google...the lifesaver for many of my problems). According to MedicineNet.com, myostatin is: "growth factor that regulates the size of muscles beginning in early embryonic development and continuing throughout life." Due to the abnormal amount of this protein in the child's body, researchers have concerns that his heart muscle could be damaged. Even though the child's cardiovascular system is fine at the moment, you can never be too sure about how it will be in following years.

After some thinking, this is not what I would call a "beneficial" mutation. Why? Well lets examine the main reason... does anyone know what will happen to the child as he grows? Most likely, the answer is NO (unless you're a psychic) because the child's future is unsure; no one is positive of how his life will unfold. Therefore, the child's gene mutation may seem advantageous now, but that could change at any moment; whether it be tomorrow, next week, or next year.

Article:

Gene Mutation Makes Tot Stronger

Chapter 14: Useful Materials

This video is from the brilliant Khan Academy. In this video, Sal explains the basics of cancer and how it is the by-product of broken DNA replication. He also explains how cancer can occur. Cancer is a disease of multicellular organisms characterized by uncontrolled cell division. It is one of the tope leading cause of death in humans!

Whenever I need to study definitions or key points, I always turn to Quizlet (CLICK HERE)! As I've mentioned before, this website has been a life saver on numerous occasions. It basically has all the needed terms and references from the chapter in the book! Therefore, this site is worth visiting for some easy studying techniques.