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Friday, April 28, 2017

Professor, please can I have more marks?

I submitted my grades on Thursday morning and they were approved by the Department of Biochemistry in short order. Once the final grades have been approved and submitted to the Faculty they can't be changed unless the change is approved by the Departmental Chair. Students may appeal their grade by paying a fee to re-read their final exam but, even then, I do not have the authority on my own to change a grade. I have to justify any change in writing. This is a good thing.

A few hours after the grades were posted I received an email message from a student [It's that time of year, again]. Here's part of what the student said,
I just saw my final mark ... which was an 76, and was very surprised. I thought I'd done well on the final exam, and had studied hard. My performance on the Midterm was good, and I had expected this to be just as well. As such, I wanted to humbly inquire whether it'd be possible to move me a 77 (a 1% increase) or even an 80. This small difference could make a very big impact on my GPA as I apply for positions to pursue a master or other professional degrees. With the mark as it is now, I fall below the GPA requirement for a program I wish to enroll in next year and will have to do another few courses or a full year to make up for it.

Friday, April 21, 2017

I'm going to Chicago!

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.



Thursday, April 20, 2017

Bill Martin is coming to town!!!

Contact me by email if you'd like to meet him on Sunday, April 30th.




The last molecular evolution exam: Question #6

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


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


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


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


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


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


Sunday, April 09, 2017

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.



Saturday, April 08, 2017

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.