Attention all Loom readers in the Cornell University area: I'm heading up to Ithaca to give a talk tomorrow on a subject near and dear to my heart--how parasites turn their hosts into puppets and slaves. I'll be at the David Call auditorium in Kennedy Hall at 4 pm. The lecture is open to the public and will, of course, include a very creepy Powerpoint. Details here, map here.
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correction. zombie carl will be appearing at cornell, giving a speech dictated by his parasites. you're not fooling anyone, parasites ... carl seems to know just a little too much about the subject
Great talk today!
The most interesting part scientifically was the question about which of a
parasite's traits are evolutionarily adaptive and which are only incidental.
The blind watchmaker's watch vs. the spandrel.
The most powerful approach to this question is genetics. Knock out or
modify the trait genetically (or find natural genetic variations), and test
whether it affects the parasitic interaction.
This approach is quite easy to do in some cases, but not (yet) in most of
the fascinating examples you discussed. It's easier for bacterial and viral
parasites (aka pathogens, same thing). Primarily because their short
generation times allow accelerated evolution. In addition some viruses like
influenza have high mutation rates and correspondingly large numbers of
progeny per generation. John Barry's The
Great Influenza is excellent about influenza virus evolution.
You didn't mention the evolution of hosts in response to the parasites.
(It was only an hour's talk.) For example the selection of hemoglobin genes
resistant to malaria's sickle-cell-anemia effects. In the world of plant
parasites there are fascinating examples of "gene-for-gene" coevolution, one
resistance gene in the host corresponding to each of the parasite's genes for
virulence, and vice versa, a coevolutionary arms war. This is an ongoing
coevolution in real time, year to year. Right now a new mutation in the wheat
parasite, stem rust, threatens to spread worldwide before plant breeders
can find and deploy a resistance gene to prevent devastation. Norman Borlaug
and millions of research dollars are involved in this effort.
- - - - - - - - - - - - - - - - - - - -
David E. Matthews, Ph.D. USDA-ARS Plant Genome Database Curator
Cornell University Email: matthews@greengenes.cit.cornell.edu
Department of Plant Breeding Phone: +1-607-255-9951
409 Bradfield Hall Fax: +1-607-255-6683
Ithaca, New York 14853, USA GrainGenes: http://wheat.pw.usda.gov
Parasitic plants are another topic you didn't have time to mention. Orobanche,
the broomrape, is amazing. A snapdragon with no leaves, nothing
green, just the showy flower spike and an organ that saps all its nutrition
from the host (tomato, sunflower, others).
How does a parasitic plant find its victims, the hosts for its next
generation? Each Orobanche flower makes thousands of tiny seeds,
nearly microscopic. These seeds sift down into the soil and wait. For
years. Until a root of their host plant grows very close, ca. 2 mm. Not
until then will the seed germinate, detecting a specific chemical exuded from
the root. The minuscule germinated root invades the host's root, and by
summer there's a fine Orobanche flower spike and a very sick tomato.
Orobanche is an economically important parasite in
some places, e.g. for tomato in Israel and chickpea in southern Europe. A
related species, Striga
(witchweed) is a serious problem for maize and sorghum in sub-Saharan
Africa, and has become established in North Carolina where eradication
efforts have been ongoing for twenty years.
Great talk today!
The most interesting part scientifically was the question about which of a
parasite's traits are evolutionarily adaptive and which are only incidental.
The blind watchmaker's watch vs. the spandrel.
The most powerful approach to this question is genetics. Knock out or
modify the trait genetically (or find natural genetic variations), and test
whether it affects the parasitic interaction.
This approach is quite easy to do in some cases, but not (yet) in most of
the fascinating examples you discussed. It's easier for bacterial and viral
parasites (aka pathogens, same thing). Primarily because their short
generation times allow accelerated evolution. In addition some viruses like
influenza have high mutation rates and correspondingly large numbers of
progeny per generation. John Barry's The
Great Influenza is excellent about influenza virus evolution.
You didn't mention the evolution of hosts in response to the parasites.
(It was only an hour's talk.) For example the selection of hemoglobin genes
resistant to malaria's sickle-cell-anemia effects. In the world of plant
parasites there are fascinating examples of "gene-for-gene" coevolution, one
resistance gene in the host corresponding to each of the parasite's genes for
virulence, and vice versa, a coevolutionary arms war. This is an ongoing
coevolution in real time, year to year. Right now a new mutation in the wheat
parasite, stem rust, threatens to spread worldwide before plant breeders
can find and deploy a resistance gene to prevent devastation. Norman Borlaug
and millions of research dollars are involved in this effort.