100th Post Blogoversary: XKCD and Dating
XKCD, the famous webcomic for nerds, has a new comic up about "dating
pools". I've heard the (age/2)+7 rule a few times before, but I've
never considered plotting it out to see what it implies. Someone found
some census data, and reports that the results are less promising than
XKCD suggests. This figure shows that, given the (age/2)+7 rule,
available singles peaks at 27.
Another figure suggests that XKCD was basically right...
Here the number of available partners does show a concave shape. Even
though I am too lazy to do the graphing, I am inclined, based on
intuition, to believe the latter curves rather than the former. I
wonder if anyone out there cares to clear up this controversy. I am
sure your paper would fly thru peer review at the venerable Annals of
Improbable Research. Just make sure you credit me as a co-author in
keeping with the guidelines for giving credit where credit is due:
Anyway, back to the graph. The situation is poor for single women past
35 yrs of age; they far outnumber single men of a similar age.
Interestingly the sex ratio at birth is 1.05:1 in favor of men. (The
genetics of sex ratio are a very interesting story, which I will cover
at some point). However, men are stupid, risk-taking fools whose
bodies tend to degenerate faster, thus women tend to live, on average,
six years longer than men. Men, that is those that haven't offed
themselves in some ridiculous stunt, will enjoy less competition for
mates once they are past the age of 35.
On the other hand, there are some folks who can mathematically
demonstrate that they will remain single for all time.
Posted by John Dennehy at 10:15 PM 2 comments Links to this post
Friday, September 7, 2007
This Week's Citation Classic
This week's citation classic is Gunther Stent's Molecular Biology of
Bacterial Viruses (WH Freeman, 1963). Stent is a polymath, currently a
professor emeriti in the MCB Department at UC: Berkeley. He started
his career by obtaining a Ph.D. in Physical Chemistry in 1948 from the
University of Illinois, then joined Max Delbruck's lab at the
California Institute of Technology, before joining the University of
California, Berkeley faculty as an Assistant Research Biochemist in
1953. Stent soon left his mark on fields as diverse as bacterial
genetics to DNA structure to neurobiology and even the history and
philosophy of science. His published books include, the classic, Phage
and the Origins of Molecular Biology (1966, 1992), the textbook,
Molecular Genetics: An Introductory Narrative, The Neurobiology of the
Leech (1981), Mind from Matter: An Evolutionary Epistemology (1986),
and his autobiography, Nazis, Women and Molecular Biology.
Molecular Biology of Bacterial Viruses is part textbook, part memoir,
part history, part lab manual and thoroughly entertaining. I still use
it and cite it in my own work. Dedicated to Max Delbruck, it opens
with a stunning photo of the DNA of phage T2 liberated from the
phage's capsid. It proceeds then to discuss phage history, morphology,
growth, life cycle, genetics and theory. Anyone with even a cursory
interest in phage cannot help being educated and entertained by this
book.
Here is a poetic tribute to Gunther Stent on the occasion of his 80th
Birthday.
Posted by John Dennehy at 12:02 PM 0 comments Links to this post
Sunday, September 2, 2007
What I did last summer (and year)....
Earlier in these pages I gave a brief background of what I've been
doing for the past year. I've been interested in how differences in
mRNA production and differences in holin structure led to variability
in lysis timing. Max Delbruck was the first to consider this question;
he looked at variation in the number of babies a single phage produces
and found a great deal of variation in this important life history
trait. Delbruck's method, diluting a suspension of infected bacteria
such each dilution contained on average less than one bacterial cell,
and then plating all the (hundreds of) dilutions, is especially
onerous, and perhaps explains why his work was not followed up.
(i.e. production rate, and observe the changes in Moreover, his work
leaves open the questions of what causes the variation and whether it
is evolutionarily significant. My work follows up on Delbruck's,
except that I chose to look at a different, but closely related life
history trait, lysis time. Earlier work has shown that there is a
direct correlation between lysis time and burst size: the longer the
phage waits to lyse the cell, the more babies it can produce. So it
makes a good proxy for burst size, as well as an interesting life
history trait in its own right. Plus, we now have the genetic
techniques to manipulate the phage's genome and dissect the causes of
variation: to wit, the ability to manipulate the holin protein
structure and to alter the strength of the promoter that controls
holin production. All we need is a way of observing lysis time for
individual cells. Enter the microscope-mounted perfusion chamber! Here
is the setup:
The way this works is you place a glass cover slip on the bottom, a
cell-binding agent (poly-lysine) and some E. coli infected with
lysogenic phage, then place another cover slip on top. The cells form
a single layer on the bottom cover slip. The whole unit is placed on a
heating platform, under a normal light microscope, and tubes are
attached to allow a flow of nutrient broth thru the chamber. The
heating platform generates a heat spike, inducing the phage to begin
the lysis process. With a microscope mounted camera, I filmed the
bound cells following the heat spike until they lysed, then recorded
the time of lysis for each cell.
Given are the variation in lysis time for the wild type (JJD3), the
most variable altered holin sequence genotype (JJD9) and the most
variable altered promoter genotype (SYP028). This histogram (below)
clearly shows the greater variability (standard deviation, SD, in
lysis time for the latter two genotypes.
In general, SD increases with the mean lysis time (below, P = 0.0087).
This result is consistent with the idea that, on average, it takes a
longer time for a weak holin-holin interaction to attain the critical
holin raft size that is necessary for hole formation. Furthermore, the
the timing of attainment also varies widely among individual infected
cells. That is, we should expect to observe a positive relationship
between the mean lysis times and their standard deviations.
Greater promoter strength leads to a shorter lysis time (P = 0.0065).
Interestingly, the lysis time variation seems to show a threshold
effect. Within a range of promoter strength (between 150 to 250),
different mean lysis times showed a similar stochasticity (P =
0.9593). However, once the promoter strength was dropped to a low
level, the stochasticity increased dramatically.
Finally I showed an environmental component to lysis time
stochasticity by reducing the nutrients provided to the host cells.
Expression of the phage holin protein requires the host synthesis
machinery, including the RNA polymerases (RNAPs) for transcription,
ribosomes for translation, and many other raw materials for protein
synthesis and enzymes for modifications. In general, cells growing at
a higher rate will have a higher concentration of the synthesis
machinery. Here as growth rate increases, the stochasticity (SD)
decreases (P = 0.0346), demonstrating that host physiology can greatly
influence the outcome of a viral infection.
The commonly invoked causes for cellular stochasticity are the random
events of gene transcription, translation, and degradation of the
expressed protein. Besides the usual causes, there is another layer of
random event for holin hole formation, namely, the association and
disassociation of holin raft on the cell membrane. However, in this
preliminary study, I was not able to attribute the relative importance
of each cause for the observed lysis time stochasticity. If the main
cause is due to host biochemistry and physiology, then it would be
difficult for the phage to reduce stochasticity. On the other hand, if
the main cause is due to the amount of holin production or holin-holin
interaction, then it is possible for mutations to change the promoter
strength or holin sequence to increase or reduce the level of
stochasticity.
Whether the observed lysis time stochasticity is evolutionarily
significant remains to be determined; however it is conceivable that
selection can favor genotypes with greater or lower levels of
phenotypic stochasticity depending on the circumstances. Future
experiments will address (1) whether variation in lysis time
stochasticity translates into variation in fitness; (2) whether
genotypes expressing greater or lower levels of lysis time
stochasticity can be selected for; (3) whether similar patterns of
stochasticity exist for different phage species.
Posted by John Dennehy at 8:26 AM 0 comments Links to this post
Saturday, September 1, 2007
Cartoons from Evolution: a journal of nature, 1927-1938
A charming archive of anti-creationist cartoons.
Noted:
Evolution:
a journal of nature
This page provides information about this otherwise lost journal in
the 1920s and 1930s devoted to promoting the teaching of evolution in
US public schools.
Maintained by:
Dr Joe Cain, Department of Science and Technology Studies, University
College London
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