Stephen Matheson

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and welcome to the 28th edition of the genetics blog carnival known as
[Mendel\'s Garden](http://mendels-garden.blogspot.com/), where we
celebrate blogging on topics related to anything touching on what Mendel
discovered (or [thought he
discovered](http://www.mendelweb.org/MWhartl.html#sD)).  
  
While reading these interesting and informative pieces, please think
about work that should be featured in a future edition and/or blogs
(like yours) that would serve well as future hosts.  
  
So do tomato seeds get you excited? No? Oh. Well, they should, if
you\'re at all interested in evolutionary genetics. Michael White at
Adaptive Complexity [explores some new
findings](http://www.scientificblogging.com/adaptive_complexity/size_matters_plants_too)
in which evolutionary changes in seed size in tomatoes are explained to
a large extent by variation in a single gene, pinpointed through the use
of standard genetic crosses. He summarizes the work as \"a clear case of
natural genetic variation controlling the size of seeds, variation for
evolution (or plant breeders) to work on when larger or smaller seed
sizes are needed to adapt to a new environment.\" Not peas, but close.
Mendel would be proud.  
  
\"[Mendel would be
proud](http://www.scientificblogging.com/ricochet_science/mendel_would_be_proud_if_he_could_get_online)\"
happens to be the title of a post by Michael at Ricochet Science,
pointing to a new educational site which he hopes will help students and
laypersons learn genetics.  
  
Ouroboros describes [experiments on an interesting DNA repair
enzyme](http://ouroboros.wordpress.com/2009/01/20/how-premature-aging-resembles-extended-longevity-part-iii/)
called Ercc1. One might think that deletion of the gene encoding this
protein (it controls nucleotide excision repair) would be a Bad Thing,
but in fact mice that have been so altered are strikingly
cancer-resistant. And there\'s more, but you\'ll have to check out the
excellent [Ouroboros](http://ouroboros.wordpress.com/) blog (focused on
aging and related biology) yourself.  
  
At the Spittoon, Erin introduces her post entitled \"[Miss
Con-GENE-iality](http://spittoon.23andme.com/2009/01/27/miss-con-gene-iality/)\"
with this teaser: \"If Facebook is starting to take over your life,
maybe your genes are partly to blame.\" The subject is heritability of
various aspects of social connectedness, and instead of whining \"I
could quit Facebook anytime I want\" just go read about these new
genetic analyses of our social behavior.  
  
On a more serious note, Razib at Gene Expression explores the [genetics
that might underlie the interesting case of Sandra
Laing](http://scienceblogs.com/gnxp/2009/01/interracial_sex_or_within_popu.php),
a woman born to apparently white parents but who appeared to be \"of a
different race.\" And in South Africa. For more on the genetics of human
appearance, see the [Eye on DNA interview with Dr. Tzung-Fu
Hsieh](http://www.eyeondna.com/2009/01/26/eye-on-dna-interview-dr-tzung-fu-hsieh-of-redtracer-dna-test-for-the-red-hair-gene-mc1r/),
developer of a test for the red hair gene.  
  
Oh, and before you give your credit card number to a personal genomics
outfit, spend some time at Genetic Future -- Daniel notes [when a
company is charging too
much](http://scienceblogs.com/geneticfuture/2009/01/cut-price_genetics_navigenics.php),
and comments on some recent remarks by [Francis Collins on the future of
\"consumer
genetics.\"](http://scienceblogs.com/geneticfuture/2009/02/francis_collins_positive_about.php)  
  
[](http://scienceblogs.com/geneticfuture/2009/02/francis_collins_positive_about.php)[Organic
transgenic
food](http://www.geneticmaize.com/2009/01/organic-transgenic-food/)
might sound like an oxymoron, but Anastasia at Genetic Maize explains
why it\'s not and introduces the new word for such methods: orgenic.  
  
Jonathan Eisen at The Tree of Life is recruiting people to help with
[analysis of metagenomic
data](http://phylogenomics.blogspot.com/2008/01/calling-all-phylogeneticists-we-need.html).
Go there to learn more. I forgot to inquire about salary and benefits.  
  
Back to evolutionary genetics: Todd at Evolutionary Novelties reports on
an [extraordinary example of evolutionary
convergence](http://evolutionarynovelty.blogspot.com/2008/12/opsins-amazing-evolutionary-convergence.html),
involving proteins called opsins which are best known for their roles in
vision.  
  
Need more evolution (with genetics)? Go read about [pink
iguanas](http://network.nature.com/people/noah/blog/2009/01/14/pink-iguanas)
at Nothing\'s Shocking. This should get you thinking about speciation,
and that means it\'s time to read about \"[speciation
genes](http://scienceblogs.com/evolvingthoughts/2008/12/some_new_work_on_speciation_an.php)\"
at Evolving Thoughts. John\'s not crazy about the term. What a grouch.  
  
And here\'s a new twist on the whole \"species boundary\" concept: Ed at
Not Exactly Rocket Science writes about a [single gene in glowing
bacteria](http://scienceblogs.com/notrocketscience/2009/02/single_gene_allows_glowing_bacteria_to_switch_from_fish_to_s.php)
that accounts for the ability of the same bacterial species to colonize
(in a mutualistic relationship) two completely different organisms
(pinecone fish with glowing \"headlights\" and squid with a luminous
\"cloaking device\"). Now that\'s cool.  
  
Let\'s give the Digital Cuttlefish the last word, at least because the
blogosphere recently treated us to [intensely disturbing images of
cuttlefish meeting violent
ends](http://scienceblogs.com/notrocketscience/2009/01/how_dolphins_prepare_the_perfect_cuttlefish_meal.php).
At that little piece of blogospheric heaven, the Digital Cuttlefish
reports on the [cuttlefish genome
project](http://digitalcuttlefish.blogspot.com/2009/01/cuttlefish-genome-project.html).
It\'s not what you think -- it\'s better.  
  
Thanks for reading, and look for the next edition of Mendel\'s Garden
the first Sunday in March at
[Biofortified](http://www.biofortified.org/).


Hello and welcome to the 28th edition of the genetics blog carnival known as Mendel's Garden, where we celebrate blogging on topics related to anything touching on what Mendel discovered (or thought he discovered).  While reading these interesting and informative pieces, please think about work that should be featured in a future edition and/or blogs (like yours) that would serve well as future hosts.  So do tomato seeds get you excited? No? Oh.

Mendel's Garden, 28th Edition

Several weeks ago, a commenter (Donald) [asked an interesting
question](http://sfmatheson.blogspot.com/2008/03/when-its-not-just-disagreement.html?showComment=1204661100000#c6790711338370489886)
about natural selection and genetic variation, and I promised to address
it because I want the issue to be a theme on QoD in the coming months.
Here\'s Donald:  

> The link below is to a NYT blog where it says that E coli studies have
> found that there are 100,000 harmful mutations for each single
> beneficial one. I\'m no population geneticist, but this kind of thing
> does make you wonder how selection could work with that much noise to
> overcome.  
>   
> That aside, I have read a little of Ronald Fisher and I recall his
> mathematical argument that for mutations of very small effect, there
> was a 50 percent chance that the net effect would be beneficial. This
> is in \"The Genetical Theory of Natural Selection\". The mutations
> with large effects, on the other hand, are almost certainly going to
> be deleterious.  
>   
> So are these studies only detecting mutations with large effects, or
> was Fisher wrong?

The [blog
article](http://judson.blogs.nytimes.com/2008/02/26/evolving-mistakes/index.html)
that Donald is citing is at [The Wild
Side](http://judson.blogs.nytimes.com/) by Olivia Judson, and the figure
of 100,000 deleterious mutants for every helpful one is widely
referenced.  
  
Donald raises two questions, which I\'ll rephrase somewhat.  
  
[1. How can natural selection lead to adaptation when there is so much
interference from harmful mutations?]{style="font-weight: bold;"}  
  
I think there are at least three misconceptions that are acting together
to create this common misunderstanding. First, that widely-cited ratio
of harmful to helpful mutations is apparently an overestimate, off by
[three orders of magnitude]{style="font-style: italic;"}, or a factor of
[1000]{style="font-style: italic;"}. The study that reported this
dramatic correction in our understanding of bacterial mutations was
published in
[[Science]{style="font-style: italic;"}](http://dx.doi.org/10.1126/science.1142284)
last August, and represents a wonderful case study of the difference
between real scientific thinking and the thinking of most design
advocates. (Subject of an upcoming post.)  
  
Second, the existence of harmful mutations doesn\'t necessarily
\"interfere\" with adaptation. Many deleterious mutations will just kill
the organism, and that\'s that. Natural selection does that all the
time, and it doesn\'t get in the way of life in general, so there\'s no
special reason to worry that it will get in the way of adaptation.  
  
But most importantly, I think Donald is a little confused about the
material on which natural selection acts, and understandably so. (This
error is the centerpiece of Michael Behe\'s ludicrous recent book [The
Edge of Evolution]{style="font-style: italic;"}.) The mistake seems
subtle, but it\'s gigantic, and I think it arises in part from a
semantic shortcut that is often used when explaining selection and
adaptation. To see the problem, consider these two alternative
descriptions of the process of adaptation.  

- Adaptive evolution occurs when natural selection favors certain
  mutations which are beneficial as opposed to harmful. When new
  challenges arise, new adaptations arise as new beneficial mutations
  are generated and selection favors these mutations.
- Adaptive evolution occurs when natural selection favors
  previously-existing genetic combinations that are more fit than
  others. When new challenges arise, new adaptations arise as selection
  favors individuals whose genetic endowments are best suited to the new
  challenges.

The first description probably sounds more familiar to you than the
second one does, but they\'re quite different, and the second
description is far more accurate than the first. The distinction between
these two scenarios lies in the implication of the first scenario that
new mutations must arise \"on demand\" or \"just in time.\" Michael
Behe\'s whole silly book is based on calculations that assume that new
mutations must be generated,
[simultaneously]{style="font-style: italic;"},
[after]{style="font-style: italic;"} the introduction of the new
challenge. (His main example is the adaptation of the malaria parasite
in the face of drugs intended for its destruction.) Those who promulgate
this error (intentionally or not) tend to emphasize natural selection
acting on [mutations]{style="font-style: italic;"}, and consequently
it\'s easy to picture a species \"mutating around\" a challenge or
obstacle. (Behe, for example, uses such language repeatedly.)  
  
But that\'s a mistaken view of the process, and the way to avoid the
trap is to picture selection acting on
[variation]{style="font-style: italic;"}, specifically on variation that
is always present in any population of organisms. (Populations without
significant genetic variation, when confronted with serious challenges,
are more likely to illustrate extinction than evolution.) Such variation
is continuously generated and therefore continuously present. This is
the lesson from studies of the effects of human selection on
[domesticated
species](http://sfmatheson.blogspot.com/2007/10/they-selected-teosinteand-got-corn.html)
of all kinds: when selection is applied, such populations typically
reveal a remarkable propensity for rapid and dramatic change, because
they harbor vast resources in the form of genetic diversity. If you
carefully attend to this distinction, you will understand Darwinian
evolution far better than any ID advocate.  
  
[2. Are most large-effect mutations harmful, and many small-effect
mutations beneficial, as predicted by
Fisher?]{style="font-weight: bold;"}  
  
Well, first of all, kudos to Donald for reading Fisher. I\'ve been
browsing [[The Genetical Theory of Natural
Selection]{style="font-style: italic;"}](http://books.google.com/books?id=sT4lIDk5no4C),
and it\'s demanding (but comprehensible). Michael Behe either hasn\'t
read it, or didn\'t understand it, and in either case is therefore
unqualified to write on evolutionary genetics.  
  
Fisher was certainly right that large-effect mutations are almost never
beneficial, but it is largely unknown whether very small-effect
mutations are frequently beneficial, as he postulated. Theoretical and
experimental work in this field has recently accelerated, and the
current model is that effects of beneficial mutations are exponentially
distributed, such that beneficial mutations are far more likely to be of
very small effect than of large effect. This was [Allen Orr\'s
proposal](http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1462510&rendertype=abstract),
and it has been borne out in some very recent experimental analyses. The
most recent, and significant, was the
[Science]{style="font-style: italic;"} paper I mentioned above, in which
the authors found that beneficial mutations in bacteria are far more
common than previously estimated, but have relatively small effects
(individually). Here\'s an excerpt from their last paragraph:  

> \...our estimate of \[the beneficial mutation rate\] implies that 1 in
> 150 newly arising mutations is beneficial and that 1 in 10
> fitness-affecting mutations increases the fitness of the individual
> carrying it. Hence, an enterobacterium has an enormous potential for
> adaptation and may help explain how antibiotic resistance and
> virulence evolve so quickly.

That\'s enough for now. Start with papers by Allen Orr when reading on
the genetics of adaption; his historical overview in [[Nature Reviews
Genetics]{style="font-style: italic;"}](http://dx.doi.org/10.1038/nrg1523)
in 2005 is particularly helpful.


Several weeks ago, a commenter (Donald) asked an interesting question about natural selection and genetic variation, and I promised to address it because I want the issue to be a theme on QoD in the coming months. Here's Donald:  The blog article that Donald is citing is at The Wild Side by Olivia Judson, and the figure of 100,000 deleterious mutants for every helpful one is widely referenced.

Postagens de Rogue Scholar

Mendel's Garden, 28th Edition

Mutations, selection, and bacteria