Viruses WERE Odd Little Things...

Awww did my title make you feel all warm and gooey inside but also made you want to read more? I know, I know. It's ok, it's ok. I understand! You ready? Off we go with some blogging!

Ok so once again viruses  have come to mind-blow us all. As we know, there is a huge debate on whether or not viruses are alive because they only contain the necessary components to reproduce, and can only do cell by invading another cell. Now viruses are generally tiny little guys, that will multiply and mess some stuff up. Please note how I said they are little things. Most viruses are much smaller than their host cells and almost fully rely on processes in the host cell to reproduce. Along came these viruses, as explained by this article, and they just kind of threw all of this previous knowledge to the wind! These things are huge! They also come chock full of lots of DNA which encodes for a bunch of proteins. One great example would be Cafeteria roenbergensis. Oh my gosh perfect time to make a joke about it being cafeteria and eating a lot so that's why it's big... But I won't. Oooh! Even better I can reference Urma!! Yeah I like that better!

Look at that an artist's rendition! I'll even give you an actual picture! Lucky you!!

Those lovely pictures were pictures of Cafeteria roenbergensis. Scientists nicknamed them CroV. Based on their size I think it's obvious what I would nickname them... So CroV is the marine largest virus known to man at the moment! It is even bigger than some bacteria! CroV has a genome of 730,000 base pairs, about 544 predicted genes, and about 22 of these genes codes for tRNA's. CroV also does something special because it takes care of its DNA just like our cells do. Many smaller viruses do not take care of their DNA in the least bit, and often exploit the mutations which occur. CroV takes care of its DNA, just like we do! Its genome encodes for DNA repair enzymes, which actively repair the virus's DNA. Scientists believe that the large size is an advantage because amoebae eat the virus and then it gets to work!
CroV falls into a class of viruses called "mimiviruses" or "giant-viruses". French scientists gave the name mimivirus because they thought the viruses were mimicking microbes. As time has gone on, scientists are finding more and more of these mimviruses all around the world, and the ocean is filled with them!

Persistent Pesky Plasmids....

You are just luh-ving the alliteration. I know, I know. I'll give you some time to simmer down.... You ready? Off we go!

Ok so this article talks about plasmids! It's kind of funny how we always learn about stuff on the BioLeague tests after the tests. I remember staring at the test and being like, "What on Earth is a plasmid..." Woe is me... But I digress! So back to the article... Yeah it talks about plasmids!

So there was a study which done to help more clearly identify the link between farm-generated animal waste and the dissemination of antibiotic resistance in microbial soil communities, by mobile genetic elements. The study used electromagnetic induction (EMI) surveying of a soil sampling that was broiler chicken farm assisted from a chicken-waste-impacted site and a not-so affected site. The EMI showed that there were differences between the two samples in pH and tetracycline resistance (Tc(R)) level in the culturable soil bacteria. Also,  several tet and erm genes were sparsely or highly present in the soil.

 Alright so here comes the interesting part. I know you're thinking, "And where are the plasmids..." So, in all of the aspects I mentioned above there really wasn't a huge difference in the marginally affected site and sites in the pristine regional forest sites. However, when the farm was operating, tet(L), tet(M), tet(O), erm(A), erm(B), and erm(C) genes were detected in the soil affected by waste. Two years after all waste was removed from the farm, tet(L), tet(M), tet(O), and erm(C) genes were still detected. Woah! If we removed them, how on earth could they still be there? Those sneaky little plasmids is how they are still there!
Being as though scientists are just constantly asking more questions, they delve even deeper and found out more information. Species of Bhargavaea, Sporosarcina, and Bacillus were the plasmid's hosts. The plasmid's mobilization (mob) gene was quantified to so they could estimte how much of it was in the soil. The ratio of tet(L) to mob changed from 34:1 at the beginning of the two years to 1:1 at the end of the two years.

Chapter 16 Helpful Hints!

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...

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!

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.

 

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.

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.

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...