Codominance vs Incomplete Dominance

I know in the beginning it says "in a minute" but, that is unfortunately a lie. This is quite the lengthy video. In this video Mr. McCammon, a teacher at Pisgah High School, teaches us the difference between codominance and incomplete dominance. This is something I was confused about. He teaches this by using punnett squares and defines and explains the functions of each term. He also briefly goes over probability and the outcomes, which is another thing I needed help with.
Briefly, codominance is when you interbreed a white and red flower and see a white and red flower. It could be striped or spotted but it is not pink. It just has patches that show both of the dominant features. On the other hand, incomplete dominance is when you would see a pink flower because it shows a blend of the two.
In sum, if you were having trouble grasping this concept I would recommend you watch this video, as it helped me.


P.S. I went to his "about" section on YouTube to see if he was legit and it said "STAR TREK: The Lost Generation" aka... yeah, he's pretty reliable :)

Why I am a BIGBOD!

This article states that I am a bigbod because... I am a girl. DAS RIGHTTTT!!!!!
This article talks about how women have stronger immune systems than men. This is because it is X-linked (as we have talked about in this chapter). Dr. Claude Libert from Ghent University in Belgium researched MicroRNA (short ribonucleic acid molecule found in eukaryotic cells that has very few nucleotides compared with other RNAs). Why microRNA? Perhaps because it is essential for all known forms of life.
"Statistics show that in humans, as with other mammals, females live longer than males and are more able to fight off shock episodes from sepsis (presence in tissues of harmful bacteria and their toxins, typically through infection of a wound), infection, or trauma", stated Libert. He claims this is because the X chromosome has 10% of all microRNA's known so far in the genome. This may be because many X chromosome- located strands of microRNA play important roles in cancer and immunity.
Dr. Libert's research states that there are biological mechanisms present on the X chromosome that play major roles on individuals' genes. Aka imprinting; and thus giving immunological advantages to females :) DAS WASSUPPPPPPP.

Le "X chromosome"

Libert's hypothesis states that he believes the immunological advantage that is present, is due to the silencing of X-linked genes by the microRNAs. "Gene silencing and inactivation skewing are known mechanisms which affect X-linked genes and may influence X-linked microRNA's in the same way"
In sum, I am a bigbod because I obvs have two X chromosomes. On the other hand, males have one X chromosome. Y chromosomes have fewer genes so if the genes involved in immunity are silenced maternally, that guy is screwed because he wouldn't have any back-up genetic information. 
Now go cry cause I'm a girl and a bigbod, and you're not!

Pedigrees Are Actually Useful?

This article talks about pedigrees! Apparently, researchers have found evidence to connect bipolar disorder to chromosome 6 and 17. They found this evidence through a pedigree series. 
First, bipolar disorder is a condition in which people go back and forth between periods of a very good or irritable mood and depression.
Prior to the actual study, researchers had reported results of a linkage analysis of bipolar disorder in what started as a set of twenty pedigrees newly discovered by the synergy of three various sites. They now report the results. They had a genome-wide linkage analysis in an independent sample of thirty-four pedigrees that separated, or sought out bipolar disorder.
Here's how: Researchers used families that were known to have a bipolar I or II disorder; individuals affected with this disorder were the first subjects in a study for the presence of bipolar I disorder, bipolar II disorder, or returning and constant major depression in a few other family members. "A total of 440 markers at an average spacing of 8 cM were genotyped in 229 family members using fluorescent methods" say researchers when 
asked about their methods.

This is a picture of chromosome 6. You can see that certain parts of this chromosome have stripes representing the different gene locations. These gene locations have names like the 6q25 region- referenced below.

In conclusion, first nonparametric analyses of chromosomes 6 and 17 proved for a simple replication of linkage to these chromosomes that had been pointed at before and speculated in previous studies. Using multipoint parametric methods, other analyses, showed further evidence to support the 6q25 region ( a region where specific genes are encoded on chromosome 6) with a heterogeneity logarithm of odds score of 3.28. From the  two-point parametric analyses we also found further evidence that again showed a simple replication of the researchers previous findings of linkage to the 23 cM region of chromosome 22q13, thus proving their theory right, further. Their results pretty much stated that there is replication of certain proven linkage peaks, like that of 6q25 and 17p12 (chromosomes 6 and 17). Other peaks from previous studies had to have not been replicated or were only modestly replicated in these analyses.

Hooray for Interactiveness!

So I just found this website that provides you with an interactive animation on mitosis, meiosis, and the cell cycle.
Check This Out!
I've linked you to the "Mitosis" page but if you look on the sidebar, you can also access "Meiosis" and "The Cell Cycle". How coolio! Aren't you glad we're friends?
This website allows you to go through all of the different phases of the cell cycle using mitosis or meiosis. You can also quiz yourself at the end to see if you're learning!
I found this website very helpful and if you are having trouble understanding these concepts, it will definitely help you in an interactive way. Especially if you're a visual/hands-on learner!

Well, the title says it all. This is quite the entertaining video. It provides a detailed explanation on the difference between mitosis and meiosis. It also gives the definitions and functions of many key terms that we have learned in this chapter. The video goes over each phase of meiosis and mitosis and also provides diagrams for each.

My Toe, Sis!

^OMG! There I go again. Making people die of laughter. If I were a potato, I'd be a funny potato. (Cred to : Thomas)

Okay, so this article gives brief overviews of mitosis, meiosis, and cell division and DNA replication as a whole. It covers the way science works and especially how the scientific method applies to biology. Then, it talks about the actual structure of the cell, building a map of the cell – knowing what processes happen where in the cell, e.g., the production of energy-rich ATP molecules in the mitochondria.

It also takes a closer look at the way DNA codes get transcribed into RNA in the nucleus (stuff we've already learned, obvi) and the RNA code translation process into protein structure in the rough endoplasmatic reticulum. Alas, it also talks about several different approaches that cells may take to communicate with each other and with the environment, thus modifying cell function.

In regards to the ways cells divide, it goes over  how cell-division, starting with a fertilized cell, builds an embryo, how genetic code (genotype) influence the observable and measurable traits (phenotype) and, finally, how these processes affect the genetic composition of the populations of organisms of the same species – the process of evolution.

This diagram shows both meiosis and mitosis. When next to each other, you can easily compare the two. They are briefly explained below.

One way mitosis is used, is for building! The process of DNA replication, as we all know, is the way all of the DNA code of the mother cell duplicates and one copy goes into each daughter cell (aka most important aspect of cell division). Other cell organelles also divide and split into two daughter cells (someone totally asked Dwebs this in class!!!!). Once the process of DNA replication is over, the new portion of the cell membrane gets built transecting the cell and dividing all the genetic material into two cellular compartments, leading the cell to split into two cells.

Meiosis is a special case of cell division. Mitosis results in the division of all types of cells in the body. Meiosis, however,  results in the formation of sex cells (the gametes: eggs and sperm). Mitosis is a one-step process: one cell divides into two. Meiosis is a two-step process: one cell divides into two, then each daughter immediately divides again into two, resulting in four grand-daughter cells. Therefore, mitosis results in two diploid cells (functional) and meiosis results in four various haploid cells (not fully functional).

Overall this is a very helpful article in briefing mitosis and meiosis :)

Me, I, Oh Sis!

Wow dat title ^ I'm hilarious. Honestly like why am I so funny? People ask me all the time...


Okay, so this article talks about variation that occurs before and after mitosis and meiotic recombination. First, what is meiotic recombination? Meiotic recombination is one of the defining events in the formation of eggs and sperm. It is a process in which DNA is exchanged between "partner" chromosomes. If the process is distrubed, chromosomes often go astray during meiotic  division, resulting in eggs or sperm with too many or too few chromosomes. In humans, the resulting embryos are almost always abnormal and are a major source of miscarriages or congenital birth defects, such as Down syndrome.

This image displays the two methods used in meiotic recombination that I have described below.

Meiotic recombination, crossovers (exchanges of genetic material between homologous chromosomes. One of the final phases of genetic recombination, which occurs during prophase I of meiosis in a process called synapsis), and gene conversions (process by which DNA sequence information is transferred from one DNA helix (remainging unchanged) to another DNA helix, whose sequence is altered; one way a gene may be mutated) all affect variation and are therefore important from an evolutionary standpoint. Crossovers increase genetic diversity by redistributing existing variation and gene converstions alter the frequency of alleles. 
A group of researches conducted a series of experiments in which they sequenced Arabidopsis Landsberg erecta (Ler) and two sets of all four meiotic products from a Columbia (Col)/Ler hybrid to try and find the genome-wide variation. This would also help them find the meiotic recombination at the nucleotide resolution. 
Their results showed many single nucleotide polymorphisms (SNPs) which are  DNA sequence variations that occur when a single nucleotide in the genome differs between members of a biological species or paired chromosomes in an individual. They also found many different sized insertions and deletions, which matched the other SNPs throughout the genome. Using a mutant, they discovered that two sets of four meiotic products were produced. They were then analyzed by sequencing in a nonfungal species. 
A total of eighteen crossovers and four gene conversions revealed that Arabidopsis gene conversions are probably fewer, and have shorter tracts, than those in yeast.
In conclusion, meiotic recombination and chromosome assortment dramatically redistributed genome variations in cells that undergo meiosis. This plays a hand in population diversity! It presents a quick way to generate copy-number variation of sequences whose chromosomes are positioned differently in both Col and Ler.

ProtoANKURgenes?

When Dwebs was going over oncogenes and protooncogenes in class, I was getting pretty confused. Thankfully this video on youtube helped me understand the difference between the two. It pretty much states that point mutations, one of the mutations we learned about, is one of the ways a protooncogene becomes an oncogene. The reason some cells become cancer cells is actually because protooncogenes become amplified. This pushes the cell towards uncontrolled growth. Another way cells become cancerous is when protooncogenes are rearranged through chromosomal translocation. This is when a gene from one chromosome is stuck to the promoter region of another chromosome. I would definitely recommend you watch this video if you were having trouble grasping the concept of protooncogenes and oncogenes.

In other news... this came up while I was on YouTube and I was like "aww, how relevant!" Not quite sure if I like it, perhaps it'll grow on me?

I Wish I Was a Dwarf!

This lengthy article is about a defective growth gene in people with rare dwarfism disorder that impedes their ability to get cancer and diabetes. This is truly miraculous considering how cancer and diabetes are two of the most common diseases that plague mankind.
Over the past few years, Jaime Guevara-Aguirre, has served as a physician in a small town in Ecuador where his patients stand at a mere 3'11". His patients have a rare genetic disorder known as Laron syndrome. A third of the world's population of people that have Laron syndrome reside in this remote village in Ecuador. What's so special about these cuties? Well, almost none of them suffer from cancer or diabetes!

This is a picture of Guevara-Aguirre (right) standing with one of his Laron syndrome patients.

These midgets have an error in their growth hormone receptor (GHR) gene which gives them their short stature. However, it also seems to keep them immune to diabetes and cancer! People who have this deficiency in growth hormone receptors are also unresponsive to growth hormone and have low levels of insulin-like growth factor 1 (IGF1). This is a hormone that promotes cell growth and inhibits programmed cell death.

Researchers conducted a series of experiments to investigate cellular response to IGF1. The studies set a precedent seeing as it was the first time that the GHR-deficiency mutation was being studied in humans. Because it is such a rare disorder, it was hard to study the subjects before. Results have shown that IGF1 can be regulated by diet aka IGF1 is an important determinant of cancer. 

In conclusion, mutations aren't always bad. Sure, people who have Laron syndrome are super short but hey, they will probably live longer and healthier lives than you will! Ain't that depressing :/

Oh, P53!

In chapter 14, we talked about tumor-supressor genes. A tumor-supressor gene is a gene that, under normal conditions, encodes a protein that prevents cancer. However, when a mutation eliminates its function, cancer may occur aka cancer-causing mutations in tumor-suppressor genes are due to a loss of activity. One tumor-supressor gene that we have talked about is p53. p53 is a transcription factor that acts as a sensor of DNA damage. It promotes DNA repair, prevents the progression through the cell cycle, and promotes apoptosis. It is present in the G1 phase of the cell cycle and controls the first checkpoint. About 50% of all human cancers are associated with mutations in this gene. This includes malignant tumors of the lung, breast, esophagus, liver, bladder, and brain, as well as leukemias and lymphomas.

This is a simple diagram that shows the pathway of p53.

This article talks about p53 and its molecular basis to chemoresistance in breast cancer. As you may have known, TP53 is the gene that encodes the tumor protein p53. Mutations in this gene have been known to be linked with resistance to anthracyclines (class of drugs used in cancer chemotherapy) and mitomycin (anticancer drug that belongs to the family of drugs called antitumor antibiotics) in breast cancer. This article goes over the possible responsibilities of different parts in the p53 cascade giving respect to drug resistance. The full article goes over the research that took place. It also talks about p53 activation in response to genotoxic stress and phsphorylations by ataxia telangiectasia mutated/ataxia telangiectasia and radiation resistance gene 3 related (ATM/ATR). Chk1 and 2 are also considered to be very important. A little while back researchers discovered that nonsense mutations in CHEK2 that encoded the chk2 protein, were found to predict resistance to anthracycline therapy in some tumors that contained wild-type TP53. As of right now, there is no evidence that MDM2 amplifications in breast cancers are resistant to anthracyclines. The roles of p53 isoforms and p53-induced transcription of non-coding RNA are yet to be determined. Experts say that disturbances affecting the p53 pathways may play key roles in chemoresistance in cancer. Although TP53 is not an exact marker for drug resistance, it still may be considered a signal for identifying critical gene cascades.