I leave tomorrow for Chicago where I'm attending Experimental Biology 2017. Is anyone else going to be there? Wanna get together? I'm there until Wednesday.
Friday, April 21, 2017
Thursday, April 20, 2017
How can alleles be fixed in a population by positive natural selection (i.e. adaptation) if the environment remains constant for thousands of years?Question #1, Question #2, Question #3, Question #4, Question #5, Question #6
Many people believe that recombination evolved because it increases genetic variation in a population and this provided a selective advantage over species that didn’t have recombination. Do you agree with this explanation for the evolution of recombination? Why, or why not? What are the other possibilities?Question #1, Question #2, Question #3, Question #4, Question #5, Question #6
More than 90% of our genome is transcribed when you add up all the transcripts from various cell types and various times of development (= pervasive transcription). Many biologists take this as evidence that most of the DNA in our genome is functional. What are the counter-arguments? Who do you believe and why?Question #1, Question #2, Question #3, Question #4, Question #5, Question #6
The Three Domain Hypothesis has eukaryotes and archaea branching off from eubacteria. It shows eukaryotes more closely related to archaea than to eubacteria. However, many scientific studies indicate that a majority of our genes are more similar to eubacterial genes than to archaeal genes. How do you explain this apparent conflict?Question #1, Question #2, Question #3, Question #4, Question #5, Question #6
The paper by Andrews et al. (2011) lists a number of common misconceptions held by their students. One of them is the idea that, “Evolution is a process that will never stop, even in the human species.” Why do they think this is a misconception? Do you agree?
Andrews, T.M., Kalinowski, S.T., and Leonard, M.J. (2011). “Are humans evolving?” A classroom discussion to change student misconceptions regarding natural selection. Evolution: Education and Outreach, 4:456-466. [doi: 10.1007/s12052-011-0343-4]Question #1, Question #2, Question #3, Question #4, Question #5, Question #6
Eugene Koonin described his view of the proper null hypothesis for evolutionary questions. One of the examples he used concerns the evolution of recent gene duplications (Koonin, 2016 p.5). Describe how one possible fate of these genes relates to constructive neutral evolution. What are the other possible fates of these genes? Which one is most likely?
Koonin, E.V. (2016) Splendor and misery of adaptation, or the importance of neutral null for understanding evolution. BMC biology, 14:114 [doi: 10.1186/s12915-016-0338-2]
... in eukaryotes, duplicates of individual genes cannot be effectively eliminated by selection and thus often persist and diverge. The typical result is subfunctionalization, whereby the gene duplicates undergo differential mutational deterioration, losing subsets of ancestral functions. As a result, the evolving organisms become locked into maintaining the pair of paralogs. Subfunctionalization underlies a more general phenomenon, denoted constructive neutral evolution (CNE).
Question #1, Question #2, Question #3, Question #4, Question #5, Question #6
Sunday, April 09, 2017
Today marks the 100th anniversary of the beginning of the Battle of Vimy Ridge. The battle invovled four divisions of the Canadian Corps and it has become a symbol for Canada of the sacrifices made during World War I. The symbol is remarkable for the beautiful Canadian National Vimy Ridge Memorial designed by Walter Seymour Allward. He intended it to be a "sermon against the futility of war."It is remarkably successful as such a symbol since, among other things, it contains the names of more than 11,000 Canadians who died in World War I and whose bodies were never recovered. We visited the memorial in 2011 with my granddaughter Zoë [Canadian National Vimy Memorial] and found the name of Lance Corporal Robert Alexander Hood, a cousin of Leslie's grandfather and Zoë's great-great-grandfather.
Saturday, April 08, 2017
A few years ago, Tomasetti and Vogelstein (2015) published a paper where they noted a correlation between rates of cancer and the number of cell divisions. They concluded that a lot of cancers could be attributed to bad luck. This conclusion didn't sit well with most people for two reasons. (1) There are many well-known environmental effects that increase cancer rates (e.g. smoking, radiation), and (2) there's a widespread belief that you can significantly reduce your chances of getting cancer by "healthy living" (whatever that is). The first objection is based on solid scientific evidence but the second one is not as scientific.Some of the objections to the original Tomasetti and Vogelstein paper were based on the mathematical models they used to reach their conclusions. The authors have now followed up on their original study with more data. The paper appears in the March 24, 2017 issue of Science (Tomasetti and Vogelstein, 2017). If you're interested in the debate over "bad luck" you should read the accompanying review by Nowak and Waclaw (2017). They conclude that the math is sound and many cancer-causing mutations are, in fact, due to chance mutations in somatic cells. They point out something that should be obvious but bears repeating.
Monday, March 27, 2017
Do you think this video is helpful? [see "What Is Evolution?"] Is it important to know that evolution requires genetic changes and that it's populations that evolve? Is it important to have a definition of evolution that covers antibiotic resistance in bacteria and blood types in humans?
Monday, March 20, 2017
Charlie McDonnell is the author of a book called Fun Science: A Guide To Life, The Universe And Why Science Is So Awesome. He made a video on misconceptions about the theory of evolution (see below). Sally Le Page (below left) is an evolutionary biologist working on her Ph.D. at Oxford (UK). She noticed a few problems with the McDonnell video so she made one of her own to correct the misconception in the first video. Now it's my turn to correct the misconception in the video that corrects the first video!Sally Le Page highlights six misconceptions in the McDonnell video. She points out that none of them are very important—they are "little niggles"—but she still thinks a comment is necessary. (I agree.)
Wednesday, March 08, 2017
I'm working (slowly) on a book called What's in Your Genome?: 90% of your genome is junk! The first chapter is an introduction to genomes and DNA [What's in Your Genome? Chapter 1: Introducing Genomes ]. Chapter 2 is an overview of the human genome. It's a summary of known functional sequences and known junk DNA [What's in Your Genome? Chapter 2: The Big Picture]. Chapter 3 defines "genes" and describes protein-coding genes and alternative splicing [What's in Your Genome? Chapter 3: What Is a Gene?].Chapter 4 is all about pervasive transcription and genes for functional noncoding RNAs.
Chapter 4: Pervasive Transcription
- How much of the genome is transcribed?
- How do we know about pervasive transcription?
- Different kinds of noncoding RNAs
- Box 4-1: Long noncoding RNAs (lncRNAs)
- Understanding transcription
- Box 4-2: Revisiting the Central Dogma
- What the scientific papers don’t tell you
- Box 4-3: John Mattick proves his hypothesis?
- On the origin of new genes
- The biggest blow to junk?
- Box 4-4: How do you tell if it’s functional?
- Biochemistry is messy
- Evolution as a tinkerer
- Box 4-5: Dealing with junk RNA
- Change your worldview
I'm working (slowly) on a book called What's in Your Genome?: 90% of your genome is junk! The first chapter is an introduction to genomes and DNA [What's in Your Genome? Chapter 1: Introducing Genomes ]. Chapter 2 is an overview of the human genome. It's a summary of known functional sequences and known junk DNA [What's in Your Genome? Chapter 2: The Big Picture]. Here's the TOC entry for Chapter 3: What Is a Gene?. The goal is to define "gene" and determine how many protein-coding genes are in the human genome. (Noncoding genes are described in the next chapter.)
Chapter 3: What Is a Gene?
- Defining a gene
- Box 3-1: Philosophers and genes
- Counting Genes
- Misleading statements about the number of genes
- Introns and the evolution of split genes
- Introns are mostly junk
- Alternative splicing
- Box 3-2: Competing databases
- Alternative splicing and disease
- Box 3-3: The false logic of the argument from complexity
- Gene families and the birth & death of genes
- Box 3-4: Real orphans in the human genome
- Different kinds of pseudogenes
- Box 3-5: Conserved pseudogenes and Ken Miller’s argument against intelligent design
- Are they really pseudogenes?
- How accurate is the genome sequence?
- The Central Dogma of Molecular Biology
- ENCODE proposes a “new” definition of “gene”
- What is noncoding DNA?
- Dark matter
Monday, March 06, 2017
I'm working (slowly) on a book called What's in Your Genome?: 90% of your genome is junk! I thought I'd post the TOC for each chapter as I finish the first drafts. Here's chapter 2.
Chapter 2: The Big Picture
- How much of the genome has been sequenced?
- Whose genome was sequenced?
- How many genes?
- Regulatory sequences
- Origins of replication
- Scaffold Attachment regions (SARs)
- Mitochondrial DNA (NumtS)
- How much of our genome is functional?