The last molecular evolution exam: Question #5

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

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The last molecular evolution exam: Question #4

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

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The last molecular evolution exam: Question #3

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

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The last molecular evolution exam: Question #2

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

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The last molecular evolution exam: Question #1

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

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Vimy Ridge

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.

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Somatic cell mutation rate in humans

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.

How to define evolution?

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?

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Correcting the correction of a video about evolution

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.)

What's in Your Genome? Chapter 4: Pervasive Transcription

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

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What's in Your Genome? Chapter 3: What Is a Gene?

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
•         Box 3-2: Yeast loses its introns
• Alternative splicing
•         Box 3-2: Competing databases
• Alternative splicing and disease
•         Box 3-3: The false logic of the argument from         complexity
• Gene families
• 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

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What's in Your Genome? Chapter 2: The Big Picture

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?
• Pseudogenes
• Regulatory sequences
• Origins of replication
• Centromeres
• Telomeres
• Scaffold Attachment regions (SARs)
• Transposons
• Viruses
• Mitochondrial DNA (NumtS)
• How much of our genome is functional?

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What's in Your Genome? Chapter 1: Introducing Genomes

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 1.

Chapter 1: Introducing Genomes

• The genome war
• What is DNA?
• Chromatin
• How big is your genome?
• Active genes?
• What do you need to know?

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Another physicist teaches us about evolution

Michio Kaku is a theoretical physicist at the City College of New York. Like many physicists, he thinks he's smart enough to know everything about everything so he doesn't hesitate to lecture people about evolution.

In this case. He's telling us that humans have reached perfection in all adaptive traits so there can't be any more selection for things like bigger brains. He tells us that human evolution has stopped because no animals are chasing us in the forest any more. He also let's us know that there are no more isolated populations because of jet planes. Watch the video to see how little he understands.



Is there something peculiar about physicists? Does anyone know of any biologists who make YouTube videos about quantum mechanics or black holes? If not, is that because biologists are too stupid ... or too smart?

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Sloppiness in translation initiation

There are two competing worldviews in the fields of biochemistry and molecular biology. The distinction was captured a few years ago by Laurence Hurst commenting on pervasive transcription when he said, "So there are two models; one, the world is messy and we're forever making transcripts we don't want. Or two, the genome is like the most exquisitely designed Swiss watch and we don't understand its working. We don't know the answer—which is what makes genomics so interesting." (Hopkins, 2009).

I refer to these two world views as the Swiss watch analogy and the Rube Goldberg analogy.

The distinction is important because, depending on your worldview, you will interpret things very differently. We see it in the debate over junk DNA where those in the Swiss watch category have trouble accepting that we could have a genome full of junk. Those in the Rube Goldberg category (I am one) tend to dismiss a lot of data as just noise or sloppiness.