Biology 2581B Lecture Notes - Cytosine, Wild Type, Erwin Chargaff

11 views3 pages

scarletrabbit663

25 Aug 2013

School

Department

Course

Professor

For unlimited access to Class Notes, a Class+ subscription is required.

Document Summary

Consider a simple game, whereby we have an unknown (x) to be a number between 1 and 100. In this way, data can only be generated by asking is the number higher or lower than x. In the first round we find that the number is higher than 10, this yields information as the number now has to be in between. In the second round, we find that the number is higher than 0, which yields no valid information as we already know that it is greater than 10 (remember that data does not necessarily equal information). In the third round we find that the number is higher than 5, which like round 2, yields no valid information. In round four we find that the number is higher than 50, which means that the number now has to be in between 51 and 100. From this simple game we can adequately define information as that which reduces uncertainty.

Related Questions

For years we have been able to analyze the fossils of extincthumans like those of Neanderthals. Their bones gave us clues to howthey looked, how they lived, and how they might be related to us.In the last few years, we have been able to get a better view intothese extinct species and their relationship to our species. Thanksto next generation genomic sequencing technologies, we have beenable to obtain genetic data on Neanderthals, Denisovans and othersthat have allowed us to make direct comparisons between our speciesand theirs. In addition, we have been able to observe the presenceof DNA from these extinct species within our own genomes which tellus that we had kids with these now extinct humans.

If we take Neanderthal DNA as an example, we find that we share99.5 percent of our DNA with them. Which means that we andNeanderthals were separated from each other for more than 500,000years. This also means that we were genetically similar enough tobe able to have offspring with each other. We see evidence of thisgenetic introgression between us and Neanderthals when we look atour DNA. Interestingly, if we obtain one thousand DNA samples fromGrossmont College students, we estimate that we would be able toextract at least 20% of the Neanderthal genome from them. Thismeans that 20% of our collective nucleotide sequences are sharedwith Neanderthals but this doesnât mean that 20% of our genes areNeanderthal specific genes. Of the twenty-one thousand genes thatNeanderthals had, only a few dozen of their genes survive withinour genome. The same holds true for Denisovans. What is moreinteresting is that older versions of ourselves have a tendency tohave higher levels of DNA from extinct humans compared toourselves. In other words, over the course of thousands of years wehave been slowly weeding out the DNA of the other humans from ourgenome in favor of our genes.

One basic question that we might like to ask is why have we beenlosing Neanderthal and Denisovan genes over time? Also, why do westill have a significant amount of DNA segments that donât seem tobe going anywhere? The answer to this has to do with selection.

The answer to the first part of the question has to do with thefact that we were not fully genetically compatible with the otherhuman species to begin with. Basically, to have had Neanderthal orDenisovan genes in the past meant that an individual's level offitness was reduced. To get rid of their genes in favor of our ownwould mean that the relative fitness of individuals would increaseovertime.

The answer to the second question has to do with the fact thatDNA segments from Neanderthals and Denisovans that did not code forproteins remained because there was little selective pressureagainst them. As far as genes are concerned, the only Neanderthaland Denisovan genes that remain only exist because they had aselective advantage or at least have been neutral to ourspecies.

DNA segments that that were neutral or that had a selectiveadvantage, whether genes or not, simply remained because they wereadvantages or there was little selective pressure against them.

Your task for this week is to look for information about oneNeanderthal or Denisovan gene that survive within our species andto tell me what function that gene has and how that gene mayincrease the fitness of modern human populations.

In your post, discussONE Neanderthal orDenisovan gene that is currently found within our species.
- Tell us about the gene and its function. Explain what it doesfor us. (Make sure you give a citation.)
- Explain in your own words any possible advantages that yourNeanderthal or Denisovan gene might have. Make sure you give ininformed opinion that is grounded in your research.

azurecrow764

GENETICS QUESTION: For this experiment we focused on forward genetics: First, his- mutants were identified and then complementation analysis was used in order to determine which of the 7 his genes was mutated. ( The exact data can be seen at the bottom). In this experiment we screened for his- mutants that were generated via a random mutation process resulting from errors in DNA replication or induced by EMS aka Ethyl methanesulfonate. We compared a mutagenized culture that was treated with EMS and an un-mutagenized culture that was not treated with EMS. However, both cultures went trhough an enrichment process to increase the frequency of his- mutants.

Point mutations involve the substitution of one type of base pair for another. If the substitution replaces a purine with a purine (or a pyrimidine with a pyrimidine), it is called a transition. If the substitution replaces a purine with a pyrimidine (or a pyrimidine with a purine), it is called a transversion. Many mutagenic chemicals cause this type of mutation by alkylation of a nucleotide base. The chemically altered base can then be misread during replication or repair. For example the mutagen, ethyl methanesulfonate (EMS), adds an ethyl (-CH2-CH3) group to both guanine or thymine bases causing the modified guanine to pair with thymine and the modified thymine to pair with guanine.

1. Why might one gene be more susceptible to EMS mutagenesis than another gene?

2. Why might we have expected to find a higher frequency of polar mutants (his4A^-B^-C^-) in the unmutagenized culture compared to the mutagenized culture?

Table 2. Experiment 1B class data summary (number of his^-mutants by section) Unmutagenized
Section	1	2	3	*4ABC*	4A	4B	4C	5	6	7	*Total his^-* mutants**
Tuesday	7	1	5	4	2	1	9	2	3	1	35
Wednesday	2	1	14	0	4	2	2	4	8	2	39
Total	9	2	19	4	6	3	11	6	11	3	74
% each mutant	12.1	2.7	25.7	5.4	8.1	4.1	14.9	8.1	14.9	4.1	~100%

Mutagenized
Section	1	2	3	4ABC	4A	4B	4C	5	6	7	*Total his^-* mutants**
Tuesday	2	5	4	2	6	5	5	0	4	1	34
Wednesday	9	1	15	0	9	1	2	2	9	4	52
Total	11	6	19	2	15	6	7	2	13	5	86
% each mutant	12.8	7.0	22.1	2.3	17.4	7.0	8.1	2.3	15.1	5.8	~100%

Please answer the question after reading the paragraph.

We have a global health challenge in our hands today, and that is that the way we currently discover and develop new drugs is too costly, takes far too long, and it fails more often than it succeeds. It really just isn't working, and that means that patients that badly need new therapies are not getting them, and diseases are going untreated. We seem to be spending more and more money. So for every billion dollars we spend in R&D, we're getting less drugs approved into the market. More money, less drugs. Now we have a whole pipeline of different organ chips that we are currently working on in our labs. Now, the true power of this technology, however, really comes from the fact that we can fluidically link them. There's fluid flowing across these cells, so we can begin to interconnect multiple different chips together to form what we call a virtual human on a chip. Now we're really getting excited.We're not going to ever recreate a whole human in these chips, but what our goal is is to be able to recreate sufficient functionality so that we can make better predictions of what's going to happen in humans. For example, now we can begin to explore what happens when we put a drug like an aerosol drug. Those of you like me who have asthma, when you take your inhaler, we can explore how that drug comes into your lungs, how it enters the body, how it might affect, say, your heart. Does it change the beating of your heart? Does it have a toxicity? Does it get cleared by the liver? Is it metabolized in the liver? Is it excreted in your kidneys? We can begin to study the dynamic response of the body to a drug. Organs on chips could also change the way we do clinical trials in the future. Right now, the average participant in a clinical trial is that: average. Tends to be middle aged, tends to be female. You won't find many clinical trials in which children are involved, yet every day, we give children medications, and the only safety data we have on that drug is one that we obtained from adults. Children are not adults. They may not respond in the same way adults do. There are other things like genetic differences in populations that may lead to at-risk populations that are at risk of having an adverse drug reaction. Now imagine if we could take cells from all those different populations, put them on chips, and create populations on a chip. This could really change the way we do clinical trials. And this is the team and the people that are doing this. We have engineers, we have cell biologists, we have clinicians, all working together. We're really seeing something quite incredible at the Wyss Institute. It's really a convergence of disciplines, where biology is influencing the way we design, the way we engineer, the way we build. It's pretty exciting.

Question: For years, technology and medicine have joined together to pave the way or even solve some of the worldâs greatest issues in healthcare. These issues include but are not limited to incurable diseases and disorders like AIDS and cancer. According to Geraldine Hamilton however, we as a population are spending too much money to develop drugs and solutions to these issues, only to be at a deficit with the drugs actually produced. She believes that one of the keys is how we test these drugs and finding more efficient ways to do so. As a result, she suggests the use of organs on chips, an innovation created and pioneered by her lab. The use of organs on chips could change the way new drugs are released and tested, thus possibly furthering the process of creating solutions to healthcareâs problems. Where is the fine line between technology and human innovation? Is human innovation gradually becoming depending on technology? (At least two paragraphs, a paragraph is at least 5 sentences long.)

Biology 2581B Lecture Notes - Cytosine, Wild Type, Erwin Chargaff

Document Summary

Get access

Related Documents

Biology 2581B Lecture Notes - Lecture 1: Guanine, Adenine, Cytosine

Biology 2581B Study Guide - Erwin Chargaff, Oswald Avery, Martha Chase

Biology 2581B Lecture 2: Lecture 2 – DNA.docx

Related Questions