Biology 2581B Final: All Lectures on Genetics Final

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 doesn’t 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 don’t 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.

*Please don't answer with photos, DO NOT UPLOAD PHOTO, it's hard to read.

I post this question twice, please don't answer this post if you already answer the other one, if you can answer different answer that's fine. REASON WHY I POST IT TWICE, I NEED TWO DIFFERENT VIEW.

Discussion

Hi All - this week you will learn about DNA - the molecule of life! You may think that protein-coding genes are the most important, but results from the Human Genome Project revealed that only about 2% of our DNA codes for protein - so what about the rest of the "junk DNA" (or non-protein coding portion of the genome) - is it functionally important? Yes! Scientists are learning how "the non-protein-coding portion of the genome is of crucial functional importance: for normal development and physiology and for disease". I would like you to please choose a topic with regards to the non-protein coding portion of the genome (this will introduce you to gene regulation which we will cover in chapter 11) or you may also choose to write about a topic that describes a mutation in any protein that is involved in DNA replication, transcription, or translation (we did not talk about all of the enzymes involved in those processes). Please list your reputable source - this is worth 0.5 pt (even if you use one of my sources below) and tell me WHY you chose your topic (this is worth 1 pt.) please try to briefly explain your topic to the best of your knowledge - I don't expect you to write a lot of detail about your topic - it might be hard to understand (which you are welcome to comment on in your paragraph)!

Examples to choose from (but not limited to) include: noncoding RNAs (snRNAs, miRNAs, siRNAs, snoRNAs, piRNAs, lincRNAs) and RNA therapeutics:

LIST:

1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119351/ (Development of microRNA therapeutics is coming of age)

2. http://www.umassmed.edu/rti/ (RNA Therapeutics Institute)

3. http://www.genengnews.com/insight-and-intelligence/rna-based-therapeutics-and-vaccines/77900520/

4. http://genesdev.cshlp.org/content/26/21/2361.full (Biology of PIWI-Interacting RNAs: new insights into biogenesis and function inside and outside of germlines)

5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4265212/ (PIWI proteins and their interactors in piRNA biogenesis, germline development and gene expression)

6. http://www.news-medical.net/news/20121203/microRNAs-play-an-important-role-during-embryonic-development.aspx

7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578617/ (the role of microRNAs in cell fate determination)

8. http://news.berkeley.edu/2017/01/13/scientists-reprogram-embryonic-stem-cells-to-expand-their-potential/

9. http://www.the-scientist.com/?articles.view/articleNo/40871/title/The-Second-Coming-of-RNAi/

10. http://web.mit.edu/newsoffice/2013/cardiac-development-needs-more-than-protein-coding-genes-0124.html (long non-coding RNA molecules)

11. http://www.alzforum.org/news/research-news/new-role-micrornas-torpedoes-sink-neurons(microRNAs)

12. http://ghr.nlm.nih.gov/condition/rothmund-thomson-syndrome (mutation in human helicase gene)

13. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3633371/ (mutation in mitochondrial helicase gene called TWINKLE)

14. http://sfari.org/news-and-opinion/news/2013/in-autism-related-disorders-rna-turns-out-to-be-key (RNA topoisomerase)

15. http://ghr.nlm.nih.gov/gene/TERC (dyskeratosis congenita - mutations in the TERC gene - the RNA component of telomerase)

16. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853347/ (Top3beta is an RNA topoisomerase that works with Fragile X syndrome protein to promote synapse formation)

The following 3 articles discuss long non-coding RNAs - there are many examples in each article so you only need to talk about one example - not the whole article:

1. http://www.sciencedirect.com/science/article/pii/S2468054016300063 (mechanism of action and functional utility)

2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5084630/ (dysregulated expression in ovarian cancer)

3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4736767/ (stem cells)