My abstract for the VW Symposium:
Anguillicola crassus is an eel-specific swimbladder nematode, which parasitizes the Japanese eel Anguilla japonica, found throughout East Asia. This species has also colonized a number of novel hosts: since the early 1980s it has spread throughout almost all populations of the European eel Anguilla anguilla, and also the American eel A. rostrata, since the 1990s. Morphological divergence of the European vs. Asian populations of A. crassus has been documented in field studies. Cross infection experiments, comparing the degree of divergence between the two nematode populations harbored in the same host species, suggest a generally decreased virulence of the European population in comparison to the Asian population, as well as differentiation of live history traits. We are currently employing new high throughput sequencing technology and analysis of gene expression data to identify the potential underlying genes for these differences, with the aim to elucidate whether divergence is driven by evolution of gene expression or coding sequence. We are also testing the "adaptationist" hypothesis that the identified genes may be involved in host-parasite interaction. Finally we will test whether these candidate genes also play a role in divergence in introduced populations of A. crassus in American eels.
Change of language, change of content
From now on this blog is about my adventures in bioinformatics and in the use of open source software:
The code is bash, perl, R -especially sweave/noweb-, LaTeX and my lovely, beastlyOS editor`s (Gnu-Emacs) elisp.
I will publish code snippets and short comments in English language. You con read about the same and my other more biology focussed interests in German on Alles was lebt.
The code is bash, perl, R -especially sweave/noweb-, LaTeX and my lovely, beastly
I will publish code snippets and short comments in English language. You con read about the same and my other more biology focussed interests in German on Alles was lebt.
Mittwoch, 29. Oktober 2008
Promoting Science-Blogging!
Ich werde Ende Februar am "VW Foundation Evolutionary Biology Status Symposium" in Muenster teilnehmen.
Es gibt die Moeglichkeit Diskussionsgruppen (auch ausserhalb streng wissenschaftlicher Themenbereiche) vorzuschlagen, als habe ich eben an die Organisatoren geschrieben:
Mal gespannt wie der Vorschlag ankommt. Das ganze boete natuerlich die Moeglichkeit zu schamloser Eigenwerbung...
Es gibt die Moeglichkeit Diskussionsgruppen (auch ausserhalb streng wissenschaftlicher Themenbereiche) vorzuschlagen, als habe ich eben an die Organisatoren geschrieben:
I have registered for the symposium a few days ago. I just had an idea for a discussion group.
"Science 2.0: Blogging as a new way of science communication"All the best,
- A blog as a medium to publish your thoughts and for scientific discussion
- Examples of the English speaking science-blogging community
- Future directions, interaction with classical ways of science communication and publishing
Emanuel
Mal gespannt wie der Vorschlag ankommt. Das ganze boete natuerlich die Moeglichkeit zu schamloser Eigenwerbung...
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Mittwoch, 22. Oktober 2008
The Brian Charlsworth quote of the week
"That`s the magic of population genetics: always take 4 times the effective population size times something!"
Sonntag, 12. Oktober 2008
The Brian Charlsworth quotes of the week
Multiple quotes, all from Thursday.
"It is like in Monty Python`s "The life of Brian": What have mutations ever done for you?"Upright walking? Increased brain size? :-)
"Fortunately the most of my genome is not doing anything...
...it`s just there for decoration!?"
...bringing a ln in the equation for the survival probability of a favourable mutation.
"So we saved the theory of natural selection from death by initial frequencies!"
We are all half dead!
This will be the first post in a new series on this blog, it will be in English and deal with papers, accompanying a course on Quantitative Genetics for Master Students. I am only voluntarily participating in this courses and try to keep up with paper discussion/essays this way...
...I will try to make the discussion both accessible for the interested reader and deep enough to meet the criteria of a good essay for the course.
Back to the topic. What do I mean with the title of this post?
With "we" I mean all animals and with "half dead" the fact that the average animal carries (heterozygote) more than one recessive allele that would be lethal if homozygote. The lethal allele has no influence on fitness of heterozygotes (half dead means fully alive here;-)) and reduces homozyygote fintness to 0.
You don`t need fancy technology to figure this out and the methods used for the study of McCune et al. are nearly as old as the field of quantitative genetics itself (the reference describing the method is in fact from 1927 and not accessible online). The experimentator mates simply siblings resulting from a cross of wild-caught animals and records the zygotes or embryos with developmental distortions leading to death. Sofar this seems facile, the only difficulty in interpretation of the reults is easy to resolve: If similar phenotyps are observed in different crosses the phenotypically healthy siblings from both crosses are outbred with each other. When all the ofspring of this controll is healthy two different recessive lethal allels were found.
This method has a single severe downside: In animals that have a reduced rate of survival as embryos or zygotes due to chance or environmental influences the experiments are not possibele. Therefore Xenopus laevis was the only vertebrate for which data on R (the number of recessive lethals per individual) was investigated by this method before. Extensive data is in contrast available on R for Drosophila.
McCune et al. found, that in both teleost fish species (Lucania goodei and Danio rerio) R is of comparable size to R in Drosophila.
The title "A Low Genomic Number of Recessive Lethals in Natural Populations of Bleufin Killifish and Zebrafish" is already part of their interpretation. They suggest that vertebrates have a higher number of genes and therefore R is smaller in relation to the number of sites that can cause lethal phenotypes.
McCune et al. infer the number of genes in their fishes from the number of genes in humans. They postulate that, because of the high synteny between vertebrates this number would be approximately the same. Unfortunately the estimation for the number of human genes was 35,000 back in 2002, the real number based on newer estimates is not higher than 25,000. The ratio of Drosophila/vertebrate genes comes down from 2.5 to 1.79 considering this.
McCune et al. propose the smaller size of vertebrate populations as a reason for the lower R (in relation to the number of genes) in vertebrates compared to invertebrates. This sounds intuitively right, because smaller populations result in higher inbreeding. For this reason selection against recessive lethal alleles would be more effective in the smaller vertebrate populations.
Nevertheless I have other doubts regarding the plausibility of the assumptions that R must be set in relation to the "exome-size". There would be no need for correcting with the number of genes, if all animals had a set of genes comparable in size, essential for their development. As R is the same in all animals the whole discussion (and the title) of the paper would make no sense in this context.
P.S. I am not aware whether vertebrates and invertebrates have this comparably large set of essential genes. It seems not to be known yet...
...or I should search harder.
Amy R. McCune, Rebecca C. Fuller, Allisan A. Aquilina, Robert M. Dawley, James M. Fadool, David Houle, Joseph Travis, and Alexey S. Kondrashov (2002) A Low Genomic Number of Recessive Lethals in Natural Populations of Bluefin Killifish and Zebrafish. Science 296 (5577), 2398.
[DOI: 10.1126/science.1071757]
...I will try to make the discussion both accessible for the interested reader and deep enough to meet the criteria of a good essay for the course.
Back to the topic. What do I mean with the title of this post?
With "we" I mean all animals and with "half dead" the fact that the average animal carries (heterozygote) more than one recessive allele that would be lethal if homozygote. The lethal allele has no influence on fitness of heterozygotes (half dead means fully alive here;-)) and reduces homozyygote fintness to 0.
You don`t need fancy technology to figure this out and the methods used for the study of McCune et al. are nearly as old as the field of quantitative genetics itself (the reference describing the method is in fact from 1927 and not accessible online). The experimentator mates simply siblings resulting from a cross of wild-caught animals and records the zygotes or embryos with developmental distortions leading to death. Sofar this seems facile, the only difficulty in interpretation of the reults is easy to resolve: If similar phenotyps are observed in different crosses the phenotypically healthy siblings from both crosses are outbred with each other. When all the ofspring of this controll is healthy two different recessive lethal allels were found.
This method has a single severe downside: In animals that have a reduced rate of survival as embryos or zygotes due to chance or environmental influences the experiments are not possibele. Therefore Xenopus laevis was the only vertebrate for which data on R (the number of recessive lethals per individual) was investigated by this method before. Extensive data is in contrast available on R for Drosophila.
McCune et al. found, that in both teleost fish species (Lucania goodei and Danio rerio) R is of comparable size to R in Drosophila.
The title "A Low Genomic Number of Recessive Lethals in Natural Populations of Bleufin Killifish and Zebrafish" is already part of their interpretation. They suggest that vertebrates have a higher number of genes and therefore R is smaller in relation to the number of sites that can cause lethal phenotypes.
McCune et al. infer the number of genes in their fishes from the number of genes in humans. They postulate that, because of the high synteny between vertebrates this number would be approximately the same. Unfortunately the estimation for the number of human genes was 35,000 back in 2002, the real number based on newer estimates is not higher than 25,000. The ratio of Drosophila/vertebrate genes comes down from 2.5 to 1.79 considering this.
McCune et al. propose the smaller size of vertebrate populations as a reason for the lower R (in relation to the number of genes) in vertebrates compared to invertebrates. This sounds intuitively right, because smaller populations result in higher inbreeding. For this reason selection against recessive lethal alleles would be more effective in the smaller vertebrate populations.
Nevertheless I have other doubts regarding the plausibility of the assumptions that R must be set in relation to the "exome-size". There would be no need for correcting with the number of genes, if all animals had a set of genes comparable in size, essential for their development. As R is the same in all animals the whole discussion (and the title) of the paper would make no sense in this context.
P.S. I am not aware whether vertebrates and invertebrates have this comparably large set of essential genes. It seems not to be known yet...
...or I should search harder.
Amy R. McCune, Rebecca C. Fuller, Allisan A. Aquilina, Robert M. Dawley, James M. Fadool, David Houle, Joseph Travis, and Alexey S. Kondrashov (2002) A Low Genomic Number of Recessive Lethals in Natural Populations of Bluefin Killifish and Zebrafish. Science 296 (5577), 2398.
[DOI: 10.1126/science.1071757]
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Dienstag, 7. Oktober 2008
The Brian Charlsworth quote of the week
Ich bin sehr froh hier in Edinburgh Vorlesungen eines der bedeutendsten lebenden Evolutionsbiologen hören zu können. Und da der gute Mann immer für einen Lacher gut ist möchte ich hier jede Woche ein Zitat präsentieren. Für letzte Woche:
Die Woche davor war der beste Satz:
"Protein-biochemists don't understand proteins"Gemeint war, dass Proteinchemiker nicht verstehen, wie (dass) Selektionsdrücke auch auf scheinbar "gleichartige" (z.B. basische AS-> basische AS) Änderungen der Aminosäuresequenz wirken können. Das Zitat gefällt mir besonders, da man an meiner Heimatuni Karlsruhe fast nur von solchen umgeben ist.
Die Woche davor war der beste Satz:
"Zoologists are generally even more stupid than geneticists"Dieser Ausspuch gehörte in den Zusammenhang, dass viele Zoologen bis Mitte des letzten Jahrhunderts noch an der Vereerbung erworbener Merkmale und an "blending inheritance" festhielten.
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