Blogging is a great way to report from a scientific conference. This could be done either with regular blog posts written in the evening or after the conference, and/or live-blogging using tools such as Friendfeed or Twitter. One or more blogging scientists can not only add a unique perspective to the reports about a conference, but for smaller conferences blogging might be the only way to learn more about a conference you were unable to attend in person.

Conference blogging (particularly live-blogging) basically requires four things:

• a wireless network,
• a computer or mobile phone with a full battery,
• a hashtag (and other tools to find the conference blog posts), and
• a blogging policy by the conference organizers.

Wireless networks are now commonplace, but enough battery power (or power outlets that conference participants can use) can be difficult. A hashtag such as #solo09 for Science Online London is essential for live-blogging using Twitter.

The big problem is the blogging policy, or rather that there usually is a policy only for traditional media, but not for blogging. The blogging from the Cold Spring Harbor Biology of Genomes meeting in May by Daniel MacArthur started a very helpful discussion about blogging policies. It is impossible to write anything specific about a conference – and that’s the stuff that is most interesting – without a permission from the conference organizer and speaker. This is best done before the conference has started. A July Nature editorial argues that an opt-out policy, where everything can be blogged about unless the speaker or poster presenter specifically says so, is a reasonable alternative.

The organizers of the Annual Meeting of the German Genetics Society that took place two weeks ago in Cologne did this right. Not only did they invite Alex Knoll to become the official conference blogger, but they also put up a prominent link to his blog posts on the conference homepage, and they asked every speaker before the conference whether Alex would be allowed to blog about their talks. Because his blog on scienceblogs.de (Alles was lebt) is in German, he decided to put up his blog posts here. I’ve asked him a few questions about this experience.

1. Did you have fun being the official blogger for the German Genetics Society Meeting?
This conference blogging job was a first for me in many ways. I usually blog in German, so I wasn’t sure if I would be able to bring more than my dry, scientific English. I also knew beforehand that there would be no theme, that the meeting was a general one. I would have at least to give the impression of having understood the basics of the talks. There would be no flitting about from talk to talk, I wanted to get whole sessions without interruption.

But on the other hand, I also got to know lots of people, many more than I would have as a lowly PhD student. I attended a conference I almost certainly would not have without the invitation to come and blog.

And, as any other (science)blogger will tell you, blogging is a labour of love (don’t stab me in the back now!). So yes, I had a great time!

2. Blogging about the conference must have been a lot of work!
About as much as I expected. I was frantically typing away at my little netbook keyboard during the talks to take notes, and used any spare time to put together the posts. So I did not have as easy a time as regular conference attendees. No problem, I came to do a job!

3. Did you meet any other science bloggers at the conference?
As far as I’m aware, I was the only blogger attending, and also the only one tweeting from the sessions (no worries, no unpublished data got out that route).

4. What was the feedback from the speakers? What was your experience getting permissions from speakers to blog about their sessions?
I got the whole range. From the really open “Go ahead! Write what you want, put it online. I’ll talk about some unpublished stuff as well, but I don’t mind” to some who are not interested in getting their work out into a blog at all. Great news for the conference blogging crowd: the balance was tipped more to the pro side! Most of the speakers came out somewhere in between those two sides, probably being a bit cautious about that whole strange blogging stuff. But I got mostly positive feedback from them, and I believe the next blogger will have an easier time when blogging about their talks!

5. What tips would you give a conference organizer who wants to promote blogging?
They should make clear from the start if blogging about the talks is generally OK. That doesn’t mean all of the speakers have to allow blogging about their talk, but an official position will help everyone involved. You also don’t need to have an official blogger, but especially at smaller meetings asking someone to blog beforehand is probably the only chance to get a blogger there at all.

I also have advice for speakers: Start your talk by telling your audience if blogging about it is OK! If a part of your talk is unpublished, tell them that as well. Or put an icon on your slides to indicate which is good to blog about, for example as Daniel MacArthur from the Genetic Future blog has proposed. If bloggers know beforehand if and what part of the talk is good to go, they will be more willing to take notes in earnest!

Now that my guest posting here at Martin’s blog comes to an end, I would like to leave you with one of the last impressions, a rather lucky shot of Cologne Cathedral I took while leaving. Many thanks to Martin for hosting this conference blog!

The final guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

Session V
Friday ended with two talks in session V, the first by Tony Hyman from the Max Planck Institute for Cell Biology and Genetics in Dresden. He looked at the ways that cells structure and organize their cytoplasm by comparison with non-biological systems.
Next up was a talk on the innate immune response against the influenza virus by University of Freiburg’s Otto Haller. When viruses infect mammalian hosts, a battle between interferons and virulence factors starts to rage. The interferon-induced GTPase Mx1 is an important resistance factor against influenza A viruses in mice. Most lab mouse strains are natural knockouts for Mx1, so they needed to create congenic, wild-type Mx1-expressing mice to research its function. Interestingly, Mx1 expression protects mice against the usually lethal 1918 Spanish flu influenza A, even at high doses. Mx proteins are highly conserved in mammalian species and belong to the dynamin superfamily of large GTPases. Otto Haller presented new and unpublished data (obtained in collaboration with Oliver Daumke´s group at the Berlin Max Delbrück Center for Molecular Medicine) on the role of the structure of the human MxA GTPase in repressing the virus.

Session VII
The final session of the meeting started with a talk by Andrew McMahon from the Harvard Stem Cell Institute in Cambridge, US, that I sadly missed. But one missed talk during the whole meeting is not that bad now, don’t you think?
Ueli Grossniklaus then talked about epigenetics in the struggle between the two parental genomes of an Arabidopsis embryo. At the University of Zürich in Switzerland, his group is looking at the timing of expression of paternal alleles and their phenotypic consequences, all controlled by the maternal genome.

The last talk was given by Bruce Beutler from the Scripps Research Institute in La Jolla, US. He is looking into the ways in which the mammalian immune system is able to recognize microbes as foreign, and then mount an adequate response. A first answer was found when the receptor for LPS, a component of all Gram-negative microbes, was identified by positional cloning as Tlr4, a Toll-like receptor. You perhaps know Toll as a developmental gene in the Drosophila embryo, but in adult flies, it is required for the immune response to fungal and bacterial infections. So perhaps other Toll-like receptors also recognize other microbial ligands? Yes, and Bruce Beutler’s group has been looking into the signalling pathways that lead from recognition by a Toll-like receptor to the induction of cellular responses. He and his group have used a forward genetic screen of randomly mutagenized mice. To date, they have generated over 100,000 mutant lines, and identified 32 mutations affecting Toll-like receptor signalling. This allowed them to deduce biochemical pathways that mediate much of the innate immune response. A similar feat was done with the genes involved in the resistance against mouse cytomegalovirus, with susceptibility mutations found in sensing and signalling pathways, but also in homeostasis and in development.

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

Saturday had two more sessions before the end of the meeting. Irina Stancheva from the Wellcome Trust Centre for Cell Biology at the University of Edinburgh started us into the day with a talk on epigenetics in mouse development.

One form of epigenetic silencing is methylation of cytosine bases in DNA. This is done by DNA methyltransferases like Dnmt1 for maintenance methylation, or Dnmt3a and Dnmt3b for de novo methylation, at CpG sequences enriched at promoters. During mouse embryonic development, DNA methylation is essential, for a loss of either of the DNA methyltransferases is embryonically lethal. Methylation and demethylation during development is surprisingly dynamic, with loss and new gain, and differences between the embryo and the trophectoderm. Besides the Dnmts, there are further proteins involved in the regulation of methylation levels. One interesting protein here is Lsh, a chromatin remodelling ATPase belonging to the SNF2 family. It seems to have a low ATPase activity in vitro, but it cooperates with several known factors like the DNA methyltransferases and Histone deacetylases. With mouse promoter microarrays, Irina Stancheva’s group compared wildtype and Lsh knockout cells, and found a reduction in promoter methylation when Lsh is missing. The patterns of DNA methylation observed in Lsh null cells suggest that this protein has a role in developmentally-programmed methylation events in the early mouse embryo.

Dominique Soldati-Favre from the University of Geneva in Switzerland gave an interesting talk about her work on apicomplexan parasites. This phylum includes important human and animal pathogens such as Toxoplasma gondii and Plasmodium falciparum causing toxoplasmosis and malaria respectively. They belong to the clade of Chromalveolates, whose ancestor acquired a plastid organelle by the secondary endosymbiosis of an alga. While some members of this clade are free living organisms or predators the Apicomplexa have evolved as obligate intracellular parasites. These parasites have developed an elaborated strategy to actively penetrate the host cells by a mechanism distinct from phagocytosis and involving gliding motility. This active mode of entry is favorable to the parasites, because this way they can evade the host cell defense mechanisms. To identify and study the molecular components of the vital process leading to host invasion, the Soldati’s group has developed genetic tools beginning from reliable DNA transfection up to the establishment of an inducible expression system for the malaria parasites based on transcription machinery elements similar to those found in plants. Studies performed on T. gondii have established that the mechanism of host cell entry is the result of a concerted action of adhesins involved in the attachment of the parasite to the host cell, the actin cytoskeleton and myosin motors that relocalize these adhesins from anterior to posterior pole of the parasite, and proteases that finally release these adhesins from the parasite surface.

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

As promised, I attended the second Plant Genetics session of the meeting, thus missing the Epigenetics session.

I learned an important lesson at the first talk by Juliette de Meaux from the Max Planck Institute for Plant Breeding Research: Bring sweets for the audience, and you have everyone on your side! Her research is on the molecular basis of variation in the life cycle of the model plant species Arabidopsis thaliana. Natural Arabidopsis strains grow in very different climates, and therefore have to adapt their annual life cycle to the environmental conditions: germinating their seeds early or late, flowering quickly after germinating or growing vegetatively for months. The ability not to germinate although there are good conditions is called seed dormancy. This can be a very important trait, for example if the Arabidopsis strain grows at a location where a short favorable period is followed by a recurring period detrimental to the growth of the plant. Then the plants which did not germinate even during the short favorable period have an advantage. But such changes in seed germination time need the whole life cycle to be fine-tuned: For the seeds of the following season to be ready before winter, the growth rate has to faster, or the flowering time shorter.
Because of the varying locations where Arabidopsis grows, there should be variation in life history strategies to be found for selection to act upon. For the model system of germination rate, Juliette de Meaux’ lab found a high variations in 180 natural genotypes they looked at. Some strains germinated at the day of harvest, while others didn’t germinate at all even 250 days after harvest, and most somewhere in between. If seeds were exposed to a cold treatment 250 days after harvest (to simulate winter), the strains that didn’t germinate after the 250 days suddenly started to germinate, while others decreased in their germination rate at longer times of cold exposure. Such and other measurements allowed for the analysis of a very complex dataset to derive the different strategies of life history in Arabidopsis. For example, there is a correlation of growth rate and flowering time to be found, but only in strains growing to the north (of Europe), not in the southern strains. They also looked at the molecular basis of this life history variation, and the consequences of it, which were interesting parts of the talk in and of themselves.

The second talk was by Rüdiger Simon from the Institute of Genetics at the University of Düsseldorf. Plants also possess stem cells, and they are located in niches (in plants called meristems) at the tips of the shoot and the root. For the shoot apical meristem (SAM), it is already known that it is composed of the stem cells and an organizing center underneath. The stem cell proliferation is regulated by a negative feedback loop: Cells in the organizing center express Wuschel, which promotes stem cell fate, but stem cells express Clavata3, that represses Wuschel via the receptors Clavata1 and Clavata2. Apart from that, there is a second negative feedback mechanism of regulating Wuschel activity known. But according to computer simulations by Rüdiger Simon and his colleagues, there are further factors needed to explain the observed distributions of cells and gene expression. They looked for such factors, and found the coryne mutant, which resembles known clavata mutants; it must be in the same pathway.
Rüdiger Simon’s lab also looked at the root tip stem cell niche, if it is perhaps also regulated by a Clavata-like pathway. Interestingly, they were able to find a Clavata3-related peptide in Cle40, that regulates the
Wuschel homolog WOX5. While this is similar to the situation in the SAM, there are also differences: WOX5 is produced in the QC, which resembles the organizing centre that expresses Wuschel , but Cle40 is not produced by the stem cells, but by already differentiated cells derived from those stem cells.

Next, Bhupendra Chaudary from Gautam Buddha University in Greater Noida, India, gave a short presentation on the fate of duplicated genes in polyploid cotton. After a genome duplication event, the evolutionary constraints on duplicated genes are relaxed, and one way change is possible is by generating differences in expression, allowing for subfunctionalization or neofunctionalization. They looked at expression differences in homoeologous genes (pairs of genes duplicated by a polyploidization event) in species of the cotton Gossypium, where parental diploid genomes as well as allopolyploids can be found. Interestingly, none of the parental genomes showed a dominant expression in the hybrids globally, but some tissue-specific transcriptional subfunctionalization.

The last talk of the session was given by Frank Kempken from the University of Kiel on mitochondrial mRNA editing in plants. Mitochondria possess their own rudimentary transcription and translation machinery, and in between they change the mRNAs in a way the nucleus doesn’t: they edit the mRNA sequence, usually by exchanging a C for an U to create novel stop codons, or to modify the amino acid sequence. How this is done is largely unknown.
Frank Kempken’s lab developed a system to work with isolated mitochondria, because genetic engineering of them in plants is not possible, and in vitro approaches have serious drawbacks. In their ‘in organello’ system, they can electroporate the isolated mitochondria in buffer, and observe the editing done to the expressed mRNAs. This allowed them to observe correct recognition of editing sites of Arabidopsis mRNAs in the mitochondria of maize, for example, or that mRNAs from chloroplasts are not edited in mitochondria. This would at least partially be expected, but somehow the plastid transcripts are not recognized by the editing machinery in the mitochondria.
Using a novel binding assay (which requires 10 liters of Arabidopsis cell culture per experiment, whew!) they were able to find proteins that bind to mRNAs at editing sites. A knockout mutant of one of them leads to growth retardation and smaller plants, exactly what one would expect when mitochondria don’t function properly anymore.

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

The last session on Thursday was split into two talks by Philippe Sansonetti from the Institute Pasteur in Paris and Julian Parkhill from the Sanger Institute in Hinxton, Great Britain. Both talked about pathogenic microbes, but from a different perspective.

After Philippe Sansonetti told us about Shigella and the innate immune system during invasion of the gut epithelium, Julian Parkhill gave us some insights into two (genomically) very different organisms. Salmonella typhi, responsible for typhoid fever, has evolved relatively recently by changing its niche; it went from being a gut pathogen to a systemic pathogen. This can be seen in its genome, because its evolution is not characterized by the gain of genes, but actually by the loss of many genes through single mutations. For bacteria, Salmonella typhi is rather strange: There is almost no recombination between strains, so there are very few SNPs that can by typed. By looking at 200 genes in about 200 strains, they found 88 SNPs in total! Evolutionarily, their data point to mostly long-term neutral mutations, with only very few genes to be found that show evidence of positive selection. But the SNP data they acquired could be put to good use nonetheless: They were able to do an epidemiological analysis in the field by collecting S. typhi strains around Kathmandu.
The opposite of S. typhi in terms of recombination and SNPs is Staphylococcus aureus, which comprises a hugely diverse group of freely recombining strains. With next generation sequencing, they were able to track the appearance and travels of a specific strain around the world. They even got enough SNPs in their dataset to be able to distinguish strains from different wards in a single hospital!
The talk was also a lesson in technological progress: While the sequencing of the Salmonella typhi genome a few years ago took 1.5 years, the next generation sequencing of Staphylococcus aureus allowed the analysis of 66 genomes per run and week. Finally, we had a glimpse into the future: They are getting into single cell genome sequencing by doing laser capture microsdissection, and are already able to reach about 98% coverage!

Following this last talk of the day, the German Genetics Society awared the honorary membership to Rolf Knippers. At least German speaking biologists should know him by name because of his well-known (and great, in my opinion) textbook Molekulare Genetik (Molecular Genetics), which first appeared in the early 1970s. But that was not the only reason for the award. Actually, Rolf Knippers has been a very good researcher and teacher, too! I didn’t know him apart from his textbook before, but the laudatio and his acceptance speech (which he started by humbly asking if he deserved the award) made me wish I had met him earlier, perhaps as a student or even as a member of his lab.

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

Both sessions had some interesting talks, so it was really hard to decide between attending Cellular Genetic Mechanisms or Human Genetics, but in the end I went to the former.

The first talk by Marina Rodnina from the Max Planck Institute for Biophysical Chemistry is not easy to put into words. Not because of a bad presentation, I should add! Her work on biochemical properties of translation involves kinetic data of a row of proteins involved in the phases of translation: initiation, elongation, termination and ribosome recycling.
I’ll give you a short summary of the initiation of translation in bacteria: First the 30S subunit of the ribosome binds a mRNA and the initiator tRNA with the help of effector proteins to form the 30S initiation complex. The 50S subunit then binds to that to form the 70S initiation complex. By fluorescently labelling all of the components of the complex, they were able to measure the rate constants (how do they bind and dissociate from the ribosome) and then calculate the binding rates to find the order of binding. This is hardest to establish for the mRNA, because of control elements like the composition of the Shine-Dalgarno sequence or secondary structures. But ignoring all of these elements, the most significant factor at this step is the mRNA concentration. Looking at secondary structure, the unfolding of the mRNA is the slow step after a quick binding. This represents a kind of stability switch to enable correct start codon recognition. Not only during initiation, but also for elongation Marina Rodnina’s lab could show that a lot of checks are kinetic in nature. Essentially, this can be summarized by the concept of induced fit: correct substrates are selectively stabilized by accelerating their forward steps.

Following was a short presentation by Matthias Schäfer on unpublished research. At the ETH Zürich in Switzerland, he is looking into the molecular role of protection against reactive oxygen species (ROS) in the epidermis.

Aria Baniahmad fom the Jena University Hospital, Germany, talked about an interesting connection of telomerase activity and androgens in prostate cancer. There, telomerase is usually active, as in many cancers to allow the cancer cell to divide indefinitely. Androgens repress telomerase activity, which is probably one reason why prostate cancer occurs later in life, when androgen levels decrease in men.
The decrease of telomerase activity is based on binding of the androgen receptor to the promoter of the catalytic telomerase subunit hTERT. In many prostate cancers, an androgen receptor with a specific point mutation can be found. This mutated AR’s binding to the telomerase promoter is weaker, which results in increased telomerase expression.

The session was closed with a talk by Thorsten Hoppe from the Institute for Genetics of Köln University, who presented intruiging, but unpublished data about his research on ubiquitin and ageing in C. elegans.

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

The first session on Friday started with a talk by Frauke Melchior from the ZMBP in Heidelberg on SUMO. Apart from being interesting to work with, it also is good for some rather funny paper titles ;-)
At the start, she gave a short introduction on the proterties of SUMO. It is similar to Ubiquitin (it stands for Small Ubiquitin-like MOdifier) and gets covalently bound to lysines of hundreds of proteins to change their protein or DNA interactions, localization, or activity. A good example I also know from my work is the yeast DNA repair helicase Srs2, which only interacts with the SUMOylated form of the replication protein PCNA at the replication fork to suppress recombination. Many protein-protein interactions that are dependent on SUMOylation can be traced back to non-covalent recognition of a SUMO-interaction motif, SIM.
Like with ubiquitin, there is an enzymatic cascade to bind a SUMO unit to a target protein; however, there is only one E1 activating and one E2 conjugating enzyme, and a handful of E3 SUMO ligases (compared to hundreds for the ubiquitin pathway). Target recognition is not understood very well, but there is a known consensus site wich is recognized by the E2 enyzme for SUMOylation. The problem is: many proteins are SUMOylated at non-consensus sites. Another mechanism turns the usual direction of the pathway on its head: The target proteins interacts with SUMO via a SIM, while it is still bound to the E2 enzyme. This allows the E2 to transfer SUMO to the target protein.
Finally, Frauke Melchior told us about an interesting pair of proteins that are involved in SUMOylation: RanGAP (RanGTPase activating protein) interacts with RanBP2 at the nuclear pore complex after it gets SUMOylated. RanBP2 itself is a SUMO E3 ligase, but not for RanGAP. Without going into too much detail (unpublished data), the story unraveled by Frauke Melchior and her coworkers showed a really complex and intriguing picture of the role SUMO plays in regulating the activity of this complex and the effect on nuclear transport.

In the second talk of the session, Chris Wylie from the Developmental Biology division of the Cincinnati Children’s hospital threw out the simple model of germ cell migration in mouse embryos found in the textbooks: During embryo development, the stem cells of the gametes, the germ line stem cells, have to migrate to their niche in the gonads. They start their travels in a structure called the allantois, go through the hindgut and from there to the genital ridges, where the gonads will form. Classically, it was thought that long range signals guide their migration. But this is problematic, because the target organ supposed to produce the guiding signal is not formed when the germ cells start their migration, and during the migration the surroundings and distances will change dramatically! That means there must be short range signals for guidance.
A nice example to test this is the trip from the midline above the gut to the genital ridges. Germ cells that stay at the midline will die by apoptosis. The previously known stem cell survival factor Steel is involved in preventing apoptosis in the cells. Its concentration decreases from the ridges to the midline; adding Steel everywhere experimentally saves the midline germ cells from apoptosis, while blocking Steel everywhere kills the germ cells laterally. They were able to show that Steel is not only involved in apoptosis, but also in the migration and proliferation of the germ cells. Steel is not only required at the late migration from the midline to the genital ridges; from the start in the allantois, loss of Steel leads to loss of germ cell number and migration.
Essentially, this means that not only is Steel one (of probably many) short range signals, but it also travels with the germ cells along their migration route, giving them a mobile stem cell niche!

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

Just after lunch the next decision: Neurogenetics or Evolution? Here I went with the topic that is less far from my field, and attended the evolution session. Welcome to the modern times, because next generation sequencing and high throughput are the way to go!

These were the methods of choice for Julia Zeitlinger from the Stowers Institute for Medical Research in Kansas City to compare transcription factor binding sites between several Drosophila species. This goes back to the question, which process contributes more to evolution: mutations in the protein-coding parts of genes, or the sequences needed for the transcriptional regulation of these genes, the so-called cis-regulatory elements. There is evidence in some organisms of a high turnover of transcription factor binding sites, and Julia Zeitlinger wanted to compare these in the genus Drosophila. This was done with chromatin immunoprecipitation approaches, where you analyze the sequence of DNA fragments to which a target protein like a transcription factor is bound. Earlier, this was followed by hybidisation of microarrays (ChIP-chip), today these DNA fragments can be directly sequenced with next generation methods (ChIP-seq). They chose the dorso-ventral patterning in the Drosophila embryo as a model system, with transcription factors like Twist that are well studied, and that have conserved binding sites. Surprisingly, they found that Twist binds to about 8 times more positions than were expected; sometimes Twist bound at more than one position at target genes.
Across Drosophila species the binding sites of Twist were very similar, especially near transcriptional start sites the positions are mostly conserved. Although movements of binding sites exist, they are rare. So it seems that there is evolutionary pressure to maintain the sites.

Also about the evolutionary contributions of cis-regulatory regions was the talk by Diethard Tautz from the Max Planck Institute for Evolutionary Biology in Plön, Germany. But he addressed them with population genetics of wild house mouse strains. With microarray and qPCR experiments, his lab was able to find that the majority of genes they looked at follow a neutral evolution. When this is not the case, most of those genes show only tissue-specific changes in expression, which points to cis-regulatory elements.
They also found a newly evolved gene in the mouse: In a region that is completely free of annotated transcripts in other mammals, one transcript can be found in the mouse. Poldi, as it is called, is expressed in the mouse testis and encodes a non-protein coding RNA. They were able to follow its birth in the genus Mus, where it appeared about 2.5 million years ago by changes in promoter regions. And although Poldi appeared relatively recently, it plays a role in the mouse. A knockout results in mice with reduced sperm motility and smaller testis, because several chromatin-regulating proteins show different expression levels in the absence of Poldi.

Now on to some computational biology by Andrew Hufton from the Max Planck Institute for Molecular Genetics in Berlin. He analyzed a special kind of cis-regulatory elements: the so-called conserved non-coding elements (CNEs), that don’t show much chance even over great evolutionary distances. Why do they exist? There are two competing hypotheses; either the CNEs repress genome rearrangements, or they promote the retention of duplicate genes nearby. To test both hypotheses, Andrew Hufton identified so-called phylogenetically conserved non-coding elements. These are elements associated with gene families and are not biased for one of the hypotheses. With experiments in zebrasish, he found that most of the PCNEs are enhancers, sequences involved in the regulation of gene expression.
Concerning the two competing hypotheses, he found a strong association between PCNE and synteny conservation – the first hypothesis: the PCNEs are enriched around genes with an ancient gene order. For the retention of duplicated genes, he showed us an alternative model.

In the last short talk of this session, Stephan Greiner told us about a plant with a strange inheritance. At the Max Planck Institute for Molecular Plant Physiology at Potsdam-Golm in Germany, he is working on the Evening Primrose Oenothera. It combines some very interesting genetic features like easy crossings between species, fertility of the resulting hybrids, biparental transmission of chloroplasts (that are usually inherited maternally) and something very strange called permanent-translocation heterozygosity: The chromosomes of Oenothera easily break at the centromeres, so that translocations of chromosome arms happen. This leads to rings or chains of chromosomes during meiosis that suppress homologous recombination and the intermixing of haploid chromosomes. In the end, there are a handful of stable genomes that a transmitted stably, and a hybrid plant with a combination of two of these genomes will always have hybrid offspring.
Add in the possibility to exchange one of several different chloroplast genomes in only two generations, and you will be able to generate compatibility charts of nuclear and chloroplast genomes, where lethal combinations and less severe phenotypes occur. Taken one step further, it is possible to identify ‘speciation genes’ in the chloroplast genome.

Another guest post by Alex Knoll reporting from the German Genetics Society Meeting in Cologne.

This time I had to decide between two parallel sessions for the first time at this meeting. Plant genetics or Development? Coming from plant molecular genetics myself, there perhaps was a ready-made decision, but I decided otherwise. There will be a second plant genetics session, and work with the axolotl and spiders lured me to the developmental biologists. But I had a rather hard time following all the new information, so please bear with me! To get at least a little bit of information about the plant genetics session, take a look into the meeting program for the abstracts (PDF)

Elly Tanaka from the Center for Regenerative Therapies in Dresden, Germany is working with the axolotl, a salamander, as her model to research the molecular and cellular events needed for spinal cord regeneration. Choosing the axolotl was a good idea because it can regenerate lots of tissues and organs, it even grows back whole legs and its tail. On the other hand, her group had to develop all of the molecular genetics fresh from the start, which was quite a lot of work I guess. But they did it, and now have EST sequences, can do single cell electroporation for gene transformations, morpholino knockdown of gene expression is possible. They were able to get transgenes transferred through the germline, can express genes in specific tissues and establish cell cultures. Quite a set, isn’t it?
This enabled Elly Tanaka’s lab to look at the events after the axolotl loses its tail by a cut, specifically how the spinal cord is able to grow back. There are two basic ideas how this is done: either it grows from the end, or it expands by cell division within the spinal cord. They found that the second hypothesis is true, because a about 500 µm long zone right after the cut gives rise to the cells of the regenerated spinal cord. By looking at molecular markers at this zone, they were able to determine that the glial cells are the progenitors for the regeneration, and they need to revert to a more primitive state.

The second invited speaker of this session, Thomas Klein from the Institute of Genetics at the University of Düsseldorf, spoke about the newly analyzed gene Lgd in the fly Drosophila melanogaster that regulates the activity of the well-known Notch gene by a new mechanism. Since this is about unpublished work, I won’t go into more detail here.

Of the three short presentations in this session, the talk of Annegret Bördlein from the Institute of Human Genetics in Erlangen, Germany, also contained essentially unpublished data.
Luckily, I am free to write about the other two talks! Thomas Widmann from the Max Planck Institute for Cell Biology and Genetics in Dresden looked at the cell shape changes in the imaginal disc in Drosophila. This structure of the fly larva will later give rise to parts of the outside of the adult body, including the wings (who would have guessed?). In the wing disc epithelium there are to cell layers that chance their shape during development: One flattens, the other elongates to columns. Thomas Widmann was able to find the two transcription factors Dpp and Wingless implicated in this shape change, since columnar cells lacking these factors are shorter. How is this done in the cell? The actin-myosin cytoskeleton builds a meshwork underneath the plasma membrane to generate tension, and the amount of force is controlled by Rho1 that can phosphorylate Myosin II. By downregulating Rho1, the cell get elongated, its overexpression shortens them. Dpp is one factor that enhances the activity of Rho1. That way, Dpp and Rho1 maintain the length in these cells.

Finally Wim Damen told us about his work on the developmental processes in the spider Achaearanea tepidariorum. At the Deparment of Genetics at the University of Jena, he is looking into segmentation processes. What happens during segmentation is very well understood in Drosophila, where a gene cascade forms all of the segments at approximately the same time. In vertebrates, the somites are comparable as a segmentation process, but here one forms after the other. Wim Damen found that in the spider, the anterior and central segments are formed like in insects rapidly and almost at the same time, but the posterior segments are formed one by one like in vertebrates. Here are even homologous genes like Notch and Wnt8 required for the segmentation. In the central region, Hunchback is essential for the production of the spider’s legs. After RNAi knockdown of Hunchback, the spiders lack some of their legs because the L1, 2 and 4 segments don’t form. This combination of insect and vertebrate-like processes during segmentation probably means that also their last common ancestor possessed both mechanisms.

Another guest post from Alex Knoll reporting from the German Genetics Conference in Cologne.

Dusko Ehrlich fom Jouy en Josas in France startet off the second session of the meeting. He is working with the MetaHIT project, which tries to do a metagenomic analysis of the human intestinal tract. This is interesting because each individual human carries about ten times more microbial cell in the gut than there are human cells in the whole body! These microbes provide the interface between the food we take in and the epithelial cells of the gut. There, they play many roles not only in metabolising materials and molecules we are not capable of, but they also produce vitamins for us and help the immune system. It is therefore very important to understand this further organ of our body, as Dusko Ehrlich called it.
The MetaHIT project takes many approaches to understand the interaction between the human intestinal microbes and human phenotypes like obesity ore bowel diseases. For example, they want to sequence a reference gene set and then look for associations of these genes with diseases. The reference gene set is produced by Solexa paired-end sequencing of samples from 124 individuals, which produced almost 0.6 terabases of sequence in total already! From these sequences contigs are produced and ORFs are predicted, which are almost completey of bacterial origin. This then allows for the comparison of bacterial genes and genomes between the sampled individuals, and also the establishment of a ‘minimal metagenome’ of the gut ecosystem for absolutely required functions.

The second talk was really interesting to me: In Drosophila melanogaster the male flies perform a courtship dance to win over the female. Barry Dickson from the Institute of Molecular Pathology in Vienna is looking for the genetic neurobiologic basis of this behaviour.
The fruitless gene, which produces a transcription factor, is absolutely required for the courtship of male flies; females don’t produce a protein product due to alternative splicing. But when females carry the male form of the fru gene, they show the typical male courtship behaviour. This means fruitless is some kind of molecular switch for male behaviour in Drosophila by programming the nervous system. So they looked at neurons that express the fru gene with the help of reporter genes and found sensory, central and motor neurons that need to be active for male courtship. Dickson’s lab was able to assemble a digital atlas of fru neurons, with stunning pictures, and were able to derive a ‘wiring diagram’. Just six easy steps: Starting from fru-expressing olfactory receptor neurons that specifically sense pheromones it only takes this few neural connections to motor output in wing muscles that are required for the courtship song!
Now the group is trying to go the high throughput route by teaching a computer to analyze the courtship behaviour by itself, and the first results look very promising.

The third talk by Andrei Lupas of the Max Planck Institute for Developmental Biology in Tübingen, Germany, was about the genetic basis of protein fold evolution. Autonomously folding units in proteins are called domains, and usually the fold of a domain is conserved with a high evolutionary permanence. Surprisingly for me, there are only about 10³ basic folds, that all were established around the time of the last universal common ancestor of all living organisms.
But there is the potential for a fold change in domains by specific alterations that go back to point mutations, deletions, insertions or recombination at the level of DNA. To understand how these changes come about, Lupas’ group is looking at experimental changes and their outcome. For example, beta-propellers are structures that arise by repeating a single ‘blade’ a certain number of times. Actually, all present beta-propellers probably all go back to one ancestral blade that was amplified several times. How large can a propeller domain become? The biggest propeller in databases has 10 blades, a 14-blade propeller in yeast forms a split between blades 7 and 8. But Lupas was able to produce a 12-bladed propeller.