Le Bioinformatics

This website is all about bioinformatics.
It talks about how the major advances and excess amounts of information needed to be organized and stored in a database, thus resulting in bioinformatics. It explains why bioinformatics is important and necessary. It provides scientists with a more global perspective in experimental design and is able to fund on the surfacing technology of database-mining (process in which testable hypotheses are generated by the function or structure of a gene or protein of interest by finding smaller sequences in better characterized organisms).
It also talks about biological databases, evolutionary biology, protein modeling, genome mapping, and tools used in bioinformatics. For example, "Map Viewer" is used to visualize whole genomes or single chromosomes.
Go check it out!

Bioinformatics: Challenge Accepted.

This article talks about some bioinformatics challenges for genome-wide association studies.
In chapter 21, we learned that bioinformatics is a field of study that uses computers, mathematical tools, and statistical techniques to record, store, and analyze biological information. to study biological information. This fast advancing branch of biology is very interdisciplinary and incorporates principles from mathematics, statistics, information science, chemistry, and physics.
We need bioinformatics because it helps us analyze an enormous amount of data in a reasonable amount of time. By sequencing the human genome, we have been able to identify over one million single nucleotide polymorphisms (SNPs) that can all be used to carry out genome-wide association studies (GWASs). New biostatistical methods have been needed for quality control, imputation, and analysis issues with multiple testing; this is because of the large amounts of GWAS data that has accumulated.
The work has had success and allowed for the discovery of new associations that have been copied in many studies. Most of the SNPs discovered through GWAS have little effects on disease susceptibility and are therefore deemed unsuitable for improving health care through genetic testing. An explanation for the mixed results of GWAS is that the biostatistical analysis example is by design agnostic or unbiased because it does not take into account the previous information on disease pathobiology. The linear modeling framework that is employed in GWAS usually only takes one SNP into account at any given time. This ignores the genomic and environmental context.
Now there is a shift away from the biostatistical approach and more towards a holistic approach. This recognizes the complication of the genotype-phenotype relationship that is set apart by significant heterogeneity along with gene-gene and gene-environment interaction.
The article goes on to assert that bioinformatics plays an important role in addressing the complexity of the
fundamental genetic basis of common human disease. The article identifies and goes into detail about the GWAS challenges that will necessitate computational methods.

Flowchart for bioinformatics analyses of GWAS data. The use of filter and wrapper algorithms along with computational modeling approaches is recommended in addition to parametric statistical methods. Biological knowledge in public databases has a very important role to play at all levels of the analysis and interpretation.

Jumping Genes in Flies

This article talks about transposable elements (TEs) that may be beneficial to fruit flies. In chapter 21, we learned that transposable elements are segments of DNA that can move from one location to another. They are inherently mobile. The ends of TEs have inverted repeats which are short DNA sequences that are present in many copies throughout the genome. All organisms contain pieces of DNA that aren't necessarily theirs, aka TEs. The finer points about factors that govern the spread of transposable elements within a population are still very unclear. The University of Veterinary Medicine, Vienna  has work that may help us increase our information about the intracellular battle that is constantly being played out between the host and invading DNA.
With new sequencing technologies, Robert Kofler and Andrea Betancourt in Schlotterer's group at the Vetmeduni Vienna's Institute of Population Genetics, were able to examine the difference in TEs in a small population of fruit flies. All the TEs in that population were catalogued. The researchers found how often TEs occur at certain sites of insertion as well.

This picture shows the function of a transposable element. It basically carries the genes and gets inserted into the bacterial chromosome.

The flies contain TEs at many sites throughout the genome despite there being many insertion sites that are actually only affected in few individuals. Researchers say that these sites were sites of recent insertion and soon we will be able to find out whether the elements are maintained there. The majority of TEs are somehow purged before they become established. Schlotterer summarized the results: "the genome is like a record of past wars between hosts and the parasitic DNA. There have been waves of attacks and the majority of them have been repelled, with only few transposable elements managing to survive and spread throughout the population."
Many sites of insertion that were more recurrent in the population than would have been expected for their age, were also found . This means that there is positive selection for TEs at these sites. This suggests that insertion has a beneficial effect on the host. 
We can conclude that TEs aren't like parasites at all, but actually very helpful. They provide organisms with an opportunity to increase their genetic collection. This is important and can be very advantageous in helping them overcome future challenges.

Plasmids

This video describes the function of plasmids. It uses diagrams and pictures to explain what plasmids do in a cell. It talks about how bacteria provide genetic engineers with restriction enzymes and plasmids. Then it talks about plasmids and restriction enzymes in further detail. Plasmids are tiny rings of DNA. Plasmids are independent and self-replicating. They allow for DNA recombination. This video is very informative regarding plasmids and bacteria. I would suggest you watch this video if you are having trouble grasping this concept.

Genetically Modified Bacteria

This article talks about how we can filter out pesticides using genetically modified bacteria.
In this chapter we learned that researchers can introduce cloned genes into oocytes, fertilized eggs, and embryonic cells to produce animals that carry the cloned genes. An organism that carries genes that were introduced using molecular techniques, like gene cloning, are called transgenic. Another name for them is genetically modified organism.
E. coli is often used in research for many beneficial experiments. Researchers have found that a genetically modified bacteria can be used in a biofilter to help remove pesticides, parathion, and methyl parathion from the air.

Biofilters use living material to capture and biologically degrade process pollutants.

A group of researchers in Beijing used a biofilter with an engineered E. coli BL21 and found the removal efficiencies of 95.2% for parathion and 98.6% for methyl parathion. Optimizing the system may allow for 100% removal. The team explained why their biofilter is better than the average, conventional biofilter. Their system was more effective, especially in the initial stages of filtering. They also explained how their biofilters work. The pesticides are broken down to p-nitrophenol as well as nitrate and sulfate byproducts. The byproducts are mineralized by other naturally occurring microbes present in the biofilter.
These two pesticides that these researchers have been focusing on are highly effective pesticides and contribute to more than a third of agricultural crop protection throughout the world. However, if they accumulate in the environment, they can seriously harm human health. This is why we are currently developing bioremediation of water and soil using bacteria that can break down these harmful compounds. These Beijing researchers focused on one aspect, air purification, using biofilters.

Baby Got BAC

^I just died for like 10 minutes. ohmygod. Why am I so funny?

This article talks about the development of a bacterial artificial chromosome recombineering procedure using galK-untranslated region for the mutation of diploid genes.
A common aim of researching genomics is to clone and analyze the entire genome of a species. For large eukaryotic genomes, it is easier when cloning vectors can accept larger chromosomal DNA inserts. Most plasmid and viral vectors can accommodate inserts that are a few thousands to tens of thousands of nucleotides in length. If a plasmid or viral vector has a DNA insert that is too large, it will have difficulty with DNA replication and is likely to suffer deletions in the insert. On the other hand, there is another type of cloning vector known as bacterial artificial chromosome (BAC). It can contain much larger inserted DNA fragments. BACs are derived from F factors, large plasmids. BACs are used in genomic research with the same use that other vectors are used for.

BAC doin' work.

BAC recombineering using galK lets cloned DNA from E. coli to be modified without letting unwanted selectable markers (gene whose presence can allow organisms to grow under a certain set of conditions) in at the modification site. Certain genomes contain pairs of inverted repeat sequences that make it difficult to bring in mutations into duplicate genes using galKs selection method. A galK-UTR BAC recombineering procedure was created to mutate duplicate genes. This procedure blocks one copy of the target duplicate gene and allows the simple mutation of the other copy. Blocked copies are now able to be replaced with a UTR-specific primer pair.
In this experiment, mutant IR2 promoters that contained three Sp-1-binding motifs and a consensus TATA box were used in place of the two IR2 promotors in EHV-1 BAC. The results from this showed that there was a 4-fold increase of the expression level of the IR2 protein. This means that the galK-UTR method will prove as a useful tool in studies of herpesviruses.

Viruses and the Lytic Cycle

This is a helpful video in which Professor George Wolfe talks about viruses, their structure, their function and their parts. The video also uses diagrams to help explain. Viruses are acellular, they have no metabolic processes, and they are parasitic. They have a capsid which is the outside layer made out of protein. The inside contains the nucleic acid. Some viruses "steal" things from their host cells. He explains that viruses are lytic or lysogenic. He walks through they lytic cycle. He explains whether or not viruses are living or non-living and goes into detail to explain why. Overall, I found this video to be very useful in explaining the function of viruses.

Prions= The Biggest of Bods :)

I'm sure you've all heard of mad cow disease? Well, mad cow disease was actually sparked by a protein called a prion. This led to fatal brain problems in the cattle. This was dangerous because it could affect any humans that ate contaminated meat. As we learned in this chapter prions are infectious proteins that cause diseases by inducing the abnormal folding of other protein molecules. So, more recently, a "mad deer" disease has come about. It targets deer, moose, and elk in the U.S. Fortunately, there are naturally occurring disinfectants found in lichen that may stop the dangerous prions in the wild.

Le Lichen (aka biggerbods than the prions)

This article talks about how lichens are natural born prion killers and how they can help us solve this dangerous disease.
These types of diseases are scary because they are produced by prions and we all know prions are super bigbods. They're super indestructible. You could be all like "aww yeahh I'm gonna boil all the bacteria outta you" and they're just like, "no". Dry heat, ionizing radiation, you name it... nothing will faze them. After all, one of the main reasons mad cow spread so fast is due to prions resistance to inactivation.
These wild animals spread the disease through their urine, feces, and saliva.
Christopher Johnson of the U.S. Geological Survey of the National Wildlife Health Center in Madison, Wisconsin, and his team found that three species of lichen have an enzyme that can break down the infamous prion!!!! Scientists concluded that when prions come into contact with lichens or soil near them, they inactivate. aka... prions are'nt so big anymore :)

Plasmids Will be the Death of Meee!!!

In this article researchers discovered that plasmids were the main reason that antibiotic resistance was spreading through bacteria. This is an important study because  more and more bacteria are resisting our antibiotics. UH OHHH! The problem is called multi-resistance. This is when an organism is able to survive even when exposed to multiple antibiotics. The antibiotic resistance can be transferred to the bacteria, even non-related bacteria, and can lead to human diseases. So how can this resistance be transferred to other bacteria, thus creating the bigger problem? Through conjugative plasmids, of course!
Conjugative plasmids help transfer genetic material between bacteria. A plasmid is a small DNA molecule that can separate from, and replicate independently of, the chromosomal DNA. These are those tiny circular things that we learned about in class.

This is picture shows the two different types of plasmid integrations into their host bacteria. The top shows non-integrating plasmids and the bottom shows episomes, where the plasmids integrate into the chromosome.

This research team studied IncP-1 plasmids. They mapped the origin of different IncP-1 plasmids and their ability to move and transfer informatoin between different species of bacteria. Peter Norberg, a researcher at IBUG stated, "Our results show that plasmids from the IncP-1 group have existed in, and adapted to, widely differing bacteria. They have also recombined, which means that a single plasmid can be regarded as a composite jigsaw puzzle of genes, each of which has adapted to different bacterial species" So the results showed that the plasmids can easily adapt. This tells us that despite the specie of 

the bacteria, these plasmids can move between and survive quickly in the different environments.

These plasmids are probably the #1 source in transferring the resistance genes between different bacteria. This is why this antibiotic resistance is becoming so widespread so fast.

In conclusion, this study showed that plasmids are the key source in spreading antibiotic resistance. It proved that IncP-1 plasmids move between different species of bacteria and interact directly with each other; thus, increasing the potential for the gene to be spread. 

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.

Mr. Anderson to the Rescue!

This is a video in which Mr. Anderson goes over gene regulation. He explains from the beginning, mentioning how E. coli is in our intestines and breaks down what we eat. He goes over and defines regulatory genes, regulatory sequences, promoters, lac operon, trp operon, transcription factors, and activators and repressors. He then carries out scenarios through diagrams so we can see how things like repressors and activators work. If you are having trouble grasping this concept, I highly recommend you watch this video!

Circadian Clock Without DNA

This article talks about two recent articles that were released recently. It goes into depth about both of the articles that have been causing quite the controversy. In both papers, both of the researchers' laboratory models were eukaryotic cells and neither had any DNA transcription or RNA translation going on inside the cell.
The results of both papers demonstrated that transcription of DNA and translation of RNA is not needed for the generation of circadian rhythms in two different types of eukaryotic cells belonging to evolutionarily very distant relatives – protists and mammals.

In the case of red blood cells, the result is lucid – there is no DNA or RNA in these cells. Thus, leaving the circadian rhythms in these cells, to be generated in the cytoplasm.

In the case of O.tauri, the picture result was a little bit more complex: the cells had a nucleus which had DNA. There was a clock driven by transcription and translation of recognized "clock genes." However, when this mechanism was supressed, by constant darkness or by chemicals, the cells still exhibited circadian rhythms generated by the molecules residing in the cytoplasm (and some of those molecules may have been strands of RNA transcribed earlier).

This is exactly what they discovered in both cases – there was a clear circadian rhythm of peroxiredoxins state-switching both in cultured red blood cells and in the cultured Ostreococcus tauri .

In sum, the phase at which the DNA-centered clock starts its cycle is determined by the phase of the cytoplasmic clock, not the other way round, i.e., the cytoplasmic clock is dominant over the nuclear clock.

Regulation of Transcription in Eukaryotes

This article talks about regulating transcription in eukaryotes. Controlling gene expression is far more complex in eukaryotes than it is in bacteria; but, they have the same basics. Eukaryotic gene expression is controlled at initiation of transcription. In bacteria, proteins control transcription. They bind to specific regulatory sequences and modulate the activity of RNA polymerase. The same thing happens in eukaryotes. The complex task of regulating gene expression in the many differentiated cell types of multicellular organisms is accomplished primarily by the synergy of multiple different transcriptional regulatory proteins. Packaging DNA into chromatin and modifying it by the process of methylation, transmit further levels of complexity to the control of eukaryotic gene expression.

This is a picture of a transcriptional activator. It has two independent domains.

This is a picture of a eukaryotic repressor. Some repressors block the binding of activators to regulatory sequences. While, others have active repression domains that inhibit transcription by interacting with general transcription factors. 

Gene expression in eukaryotes is regulated by transcriptional activators and repressors. Activators bind to regulatory DNA sequences and stimulate transcription. They appear to be modular proteins. So, the DNA binds and activates domains of different factors and thereby these factors can frequently be interchanged using different DNA techniques. Repressors on the other hand, bind to specific DNA sequences. I like to think of them as inhibitors. In most cases, eukaryotic repressors interfere with the binding of other transcription factors to DNA. For example, when a repressor binds near the transcription start site, it can block the interaction of RNA polymerase (or general transcription factors) with the promoter. Other repressors compete with activators for binding to specific regulatory sequences.