As you might expect, losing the entire semester's worth of writing and the first month of summer for research really did not leave much room for anything else. I spent most of the time that I was in lab on my feet skating around everyone else to check optical densities or make time points or to do any of the other work that needed to be done at the time. What this meant was that I didn't have time to stay current regarding the articles in my field or to begin reading up on the parts of my research that had changed since my first project was cut short. So, a couple days ago when things started to wind down a little bit that's exactly what I did.
My original project was titled "Characterization of ribonucleoprotein (RNP) granules in yeast exposed to fermentation inhibitor furfural." The benefit of this project was that it was relatively straightforward but had the potential to produce some pretty fundamental information to the fields of cell and molecular biology. Basically all I had to do was transform the P-body and stress granule marker plasmids into the yeast and grow them in the presence of furfural, periodically preparing slides from the culture to look at under fluorescence microscopy for formation for the RNPs. I admit it was pretty simple stuff, but it was engaging enough for my first project.
After I ended that project, the new focus of my research became comparative in nature. Whereas before I was only concerned with whether RNPs formed, now that we know they do in the presence of furfural (thanks, Iwaki), I am tasked with seeing if the overexpression of ZWF1, a gene important in the pentose phosphate pathway, effects their formation in the yeast. There is good reason to think that it will, but that's for another post.
So there I was consulting genome databases and the latest articles on ZWF1 when I come across an interesting piece of information: yeast ZWF1 is a homolog to a gene in humans. That is, humans have the same gene which is involved in the same relative process.
So here's where it gets sciencey. Brace yourselves.
ZWF1 in both humans and yeast codes for a protein, zwf1p, better known as glucose 6-phosphate dehydrogenase (G6PD). G6PD is an enzyme that catalyzes the first step - the rate-determining, irreversible one - in the pentose phosphate pathway, a mechanism which reduces NADP+ to NADPH. Basically, these activated carrier complexes are vital for cells - whether human or yeast - because they comprise one of the only methods biological organisms have for dealing with oxidative stress. So, NADPH reduces a molecule called glutathione. Reduced glutathione acts as a mop for free radicals in the system, removing the pressure of the oxidative stress, which is all well and good, but that's only part of why ZWF1 is so interesting.
Often in organisms diseases or afflictions amount to problems with a single gene or protein. Such is the case with hemolytic anemia, or G6PD deficiency. Hemolytic anemia is the result of a person having a low RBC count. There can be many things that case this but with G6PD deficiency, the resulting hemolytic anemia is caused by, you guessed it, a problem with G6PD - the enzyme that is coded from ZWF1, the gene whose homolog I work with in yeast. From what I understand, some event results in relatively inactive G6PD, which means a halted pentose phosphate pathway, which means no reduction of NADP+ to NADPH, which means no reduction of glutathione, which means its a free radical family reunion up in that cell. Further, erythrocytes have no other mechanism for dealing with oxidative stress -they rely solely on the pentose phosphate pathway, so those sucker just burst from all that stress resulting in the low RBC count a.k.a. hemolytic anemia.
Point is, unannounced to me, I've been working on some pretty rad medical stuff in addition to the implications overexpression of ZWF1 has on fermentation.
Fucking intense, am I right?
After I ended that project, the new focus of my research became comparative in nature. Whereas before I was only concerned with whether RNPs formed, now that we know they do in the presence of furfural (thanks, Iwaki), I am tasked with seeing if the overexpression of ZWF1, a gene important in the pentose phosphate pathway, effects their formation in the yeast. There is good reason to think that it will, but that's for another post.
So there I was consulting genome databases and the latest articles on ZWF1 when I come across an interesting piece of information: yeast ZWF1 is a homolog to a gene in humans. That is, humans have the same gene which is involved in the same relative process.
So here's where it gets sciencey. Brace yourselves.
ZWF1 in both humans and yeast codes for a protein, zwf1p, better known as glucose 6-phosphate dehydrogenase (G6PD). G6PD is an enzyme that catalyzes the first step - the rate-determining, irreversible one - in the pentose phosphate pathway, a mechanism which reduces NADP+ to NADPH. Basically, these activated carrier complexes are vital for cells - whether human or yeast - because they comprise one of the only methods biological organisms have for dealing with oxidative stress. So, NADPH reduces a molecule called glutathione. Reduced glutathione acts as a mop for free radicals in the system, removing the pressure of the oxidative stress, which is all well and good, but that's only part of why ZWF1 is so interesting.
Often in organisms diseases or afflictions amount to problems with a single gene or protein. Such is the case with hemolytic anemia, or G6PD deficiency. Hemolytic anemia is the result of a person having a low RBC count. There can be many things that case this but with G6PD deficiency, the resulting hemolytic anemia is caused by, you guessed it, a problem with G6PD - the enzyme that is coded from ZWF1, the gene whose homolog I work with in yeast. From what I understand, some event results in relatively inactive G6PD, which means a halted pentose phosphate pathway, which means no reduction of NADP+ to NADPH, which means no reduction of glutathione, which means its a free radical family reunion up in that cell. Further, erythrocytes have no other mechanism for dealing with oxidative stress -they rely solely on the pentose phosphate pathway, so those sucker just burst from all that stress resulting in the low RBC count a.k.a. hemolytic anemia.
Point is, unannounced to me, I've been working on some pretty rad medical stuff in addition to the implications overexpression of ZWF1 has on fermentation.
Fucking intense, am I right?
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