lpotter's blog

The conclusions that can be drawn from the results is that Sulfolobus Spindle Shaped Virus (SSV) developed an escape mutation whenever a dip in the bacterial population of Sulfolobus was observed. This means that at any of these instances the SSV was able to mutate to again be able to kill the Sulfolobus. On the graph when there was more diversity and distribution within the immune systems of Sulfolobus the bacterial cells were significantly less susceptible to SSV infection. From the results it can also be concluded that Sulfolobus and SSV have a mutualistic relationship. The SSV uses host machinery to create and secrete a toxin that kills healthy uninfected cells. This also implies that infected cells are immune to the toxin is that the SSV provides infected cells with an antitoxin keeping them safe. This relationship is considered mutualism because the bacterial cells essentially want to be infected in order to survive.

The conclusions that are drawn from these results is that SSV developed an escape mutation whenever a dip in the bacterial population of Sulfolobus was shown. This means that at any of these instances the SSV was able to mutate to again be able to kill Sulfolobus. On the graph when there was more diversity and distribution within the immune systems of Sulfolobus the bacterial cells were significantly less susceptible to SSV infection. The conclusion relating to the Sulfolobus and SSV having a mutualistic relationship is something that I have never seen nor thought about before. The SSV uses host machinery to create and secrete a toxin that kills healthy uninfected cells. The conclusion as to why infected cells are immune to the toxin is that the SSV provides infected cells with an antitoxin keeping them safe. This relationship is considered mutualism because the bacterial cells essentially want to be infected in order to survive. A conclusion about P. aeruginosa infections in humans with chronic CF is that each human is an island population that host the P. aeruginosa and a phage with an anti-CRISPR system which has ways of making CRISPR immunity less effective.

The results showed that there were many aspects as to how cells maintain a uniform rod shape as they grow. One result showed that there are two main ways that new cell wall is added to the cell. The first being that new cell wall is inserted in an oriented manor, which means that filaments travel around the radius of the cell and are oriented by cell radius rudders. The second is that new cell wall is inserted in an unoriented manor, this means that cell wall is inserted randomly by enzymes. Another result showed that when mreBCD was upregulated the cell rod width decreased and it became skinnier, if mreBCD was downregulated then the cell rod width increased and it became fatter. The salt shock showed that cells with upregulated mreBCD were able to maintain their rod form for a longer time than cells with lower levels. An additional result showed that when the cells were provided additional nutrients they were able to grow into a rod shape quicker. A similar result showed that when the cell was essentially tricked into thinking it had adequate nutrients it grew at the same rate showing that a kinase domain was responsible for sensing environmental nutrients.

Quorum sensing is something that bacterial cells can use to communicate. The signals that the bacteria produce are N-acyl-homoserine lactones or AHLs. These signals can be received by the bacterial species or different bacterial species. There are two primary genes involved in quorum sensing. There is the I gene which codes for AHL synthase and the R gene which is a transcriptional regulator. AHL synthase, which the I gene codes for, is responsible for producing the AHL signal that other bacterial cells will be able to receive. The AHL binds to a receptor on a neighboring cell and a transcriptional response is activated, this is where the R gene begins to function. The R gene transcribes new DNA in response to the signal being received. For example the bacteria C. violaceum produces a purple pigmented antibiotic violacein, C. violaceum only produces this antibiotic after it has received a signal from a neighboring cell telling it to do so. Quorum sensing is vital for bacteria living in the environment to communicate with neighboring cells.

Quorum sensing is something that bacterial cells can use to communicate. The signals that the bacteria produce are N-acyl-homoserine lactones or AHLs. These signals can be received by the bacterial species or different bacterial species. There are two primary genes involved in quorum sensing. There is the I gene which codes for AHL synthase and the R gene which is a transcriptional regulator. Both of these genes are very unique and serve many functions. They both have two main functions though. AHL synthase, which the I gene codes for, is responsible for producing the AHL signal that other bacterial cells will be able to receive. The AHL binds to a receptor on a neighboring cell and a transcriptional response is activated, this is where the R gene begins to function. The R gene transcribes new DNA in response to the signal being received. For example the bacteria C. violaceum produces a purple pigmented antibiotic violacein, C. violaceum only produces this antibiotic after it has received a signal from a neighboring cell telling it to do so.

The new england aquarium just opened a new coral reef tank. It looks absolutely incredible. The reef is set to mimic an indo-pacific coral reef. It holds 9000 gallons of water and spans from the floor to the ceiling. Coral reefs have always been fascinating to me because of how diverse and colorful they are. I have been snorkeling over a reef once and was scared the entire time. I am scared very easily in the water, I just feel like I am too far out of my element. Anything that is in the water can move easily in it, except for things that don’t belong there, like me. I love how beautiful the ocean is and how unique all of the creatures that inhabit it are. The ocean is just too big of a jump for me to make, just knowing how easy it would be for anything in the ocean to cause harm to me. On a separate note I really want to see the coral reef at the aquarium. First because I doubt I will ever be able to a reef of this nature in real, and secondly because even if I did like swimming in the ocean reefs like these may be gone by the time I have the means to visit one.  

I just did the weekly preparation assignment about poster assessment. The poster that I looked at tried to find a link between google searches for west nile virus and if the virus was present in the area. It was a pretty cool idea, they had an algorithm to predict when and where the next west nile outbreak would be but when they incorporated google trends into the algorithm it became significantly more accurate. The researchers best guess as to why this could be is because if people here about the virus or there are a lot of mosquitoes present people search for the virus. The more people searching it in a specific area is usually fueled by a certain factor. The poster looked very nice overall, it had all of the components that a scientific poster requires. I was not a huge fan of the way that the poster flowed through. It appeared broken up by the two figures in the middle of the poster and the text was in two sections on either side that had little separation. This made it look like there were two massive blocks of text on either side of the poster, that kind of through off the flow when I read it.

Bacteriophages also have another type of life cycle. It is called the lytic cycle, the purpose of this life cycle is to rapidly replicate, lyse the cell, then package it’s DNA to go to a bacteria and infect another one. The lytic cycle has the bacteriophage replicate it’s DNA rapidly while making packaging for that DNA. The packaging includes the head and tail of the bacteriophage, this will keep the DNA safe until it gets to the next bacteria that it will infect. It also has to package it in a way that the bacteriophage will be able to insert its DNA into the next bacterial cell that it infects. This is a very interesting process. The goal of this process is to make as many bacteriophages as possible, this will allow the bacteriophages to leave the host cell and infect a bunch of other host cells. There are many proteins that the bacteriophage carry with them to make packaging for their DNA. And like in the lysogenic life cycle some bacteriophage use the host proteins to create their own packaging. Bacteriophages really are interesting, they infect bacteria which can infect us. There are viruses for everything, they can infect everything in life. The only thing that can’t be infected by a virus is a virus itself, and that is only because they can’t replicate on their own.

Bacteriophages might be one of the coolest things in all of the natural world. They are viruses that infect bacteria. Bacteriophages are the pictures you see that look like an alien spaceship landing on a cell surface. They send their DNA into the bacterial cell. They can go through 2 separate life cycles, lytic and lysogenic. The lysogenic life cycle of the bacteriophage is for replicating DNA as fast as possible within the cell. What this means is that the bacteriophage replicates it’s own genome within the host cell replication machinery. Other types of bacteriophages package their own replication machinery so they don’t have to borrow it from the host cell. I think that packaging their own replication machinery is significantly less common than borrowing it from the host cell. It is more efficient for the bacteriophage to borrow the replication machinery from the host because it doesn’t have to waste space carrying it to the next host cell if it is already there. Typically during the lysogenic cycle DNA from the bacteriophage is inserted in to the bacterial genome. This is sometimes how genes are passed from bacteria accidentally. It is a really interesting process and sometimes drug resistance accidentally gets passed from bacteria to bacteria.

I have a microbiology exam tomorrow which I have yet to study for. There is way too much information to start now. We have to know a paper by someone who’s last name is Brenner, why we have to know a paper from the 50’s I have no idea. The paper is interesting, it is about proving that DNA codons are in triplets. He does this by doing a few math computations that are very simple. The only reason that the paper has any relevance is that he was the first to publish this thought. It didn’t prove anything about how codons work or their importance. It just proves that codes come in sets of 3 nucleic acids. This is a very informal paper and it almost just seems like the author typed up what he was just scribbling down on his desk one afternoon. I really don’t understand why we need this for our test and why this is important to the class that I am taking. I already know that codons are in sets of three, this has been repeatedly taught in almost all of my science courses since high school. The paper doesn’t even necessarily prove what codons are, it just proves that based off other properties that they most likely function in groups of 3.