CharonY

Uhhh that is perfect.

I want a swansont bobblehead on my desk.

The analogy fails in many aspects, especially considering the improvement of health outcomes e.g. quantified by life expectancy. Other examples besides vaccines are antibiotics that actively destroy the causative agents of the disease and whose negative effects vanish after the treatment (together with the disease) etc. Also, this belongs into speculations.

It is cartilage that is growing. Not a functioning ear. And it is way off from an artificial organism. To add more details, it was a scaffold implanted into the mouse and seeded with cartilage cells. None of which were even remotely human. So neither genetic manipulation was conducted nor was human material used. Again, the things people know...

IIRC the UCSC Genome Browser had only a limited amount of species (maybe they updated it by now, I am not sure). One simple way to extract the sequence is, simply to go into the genome browser from NCBI for the respective organism, note the start and end position and just export a few hundred bp up and down from there. I think they updated quite a lot of stuff and there may now actually be an easier way to do so. I generally used download the sequences and used custom tools to play around with it. Of course there is also the possibility to download the sequences and open it up in one of the freeware genome browser (e.g. artemis) and extract your stuff from there. It really depends what you want to do. Just a thought, if you want to compare the whole regions of the organisms, you may also want to look e.g. at synteny.

Virus are not cells but mostly protein plus nucleic acids, prions are just extremely small proteins. Unlike viruses prions do not replicate but change existing prions. Nonetheless even they require water to function. And indeed there are no strict definitions of life. Most are of the post hoc variety.

This is unlikely to work. The sum would have to be enormous to be any incentive at all. Certainly in the billions of dollar range. And even then given low potential to being awarded the price (as opposed to, say, selling a new flavor of cough medicine) the expected return for any investment is too low. What nec209 posted has some truth in it, though. One of the arguably best way to save lives is to improve on diagnostics. However, there is little incentive from the pharmaceutical side to develop them as a the revenue from diagnostics is abysmally low compared to the development cost. Incidentally that was one of the major points in a biomarker conference recently. Of course one could do both, use government money to develop life saving but less lucrative diagnostics and medicine. However, the required investment would be huge. Already the NIH and similar funding agencies are pouring money into explorative uni research, however the grants that they give out are usually insufficient to conduct the big trials necessary to push things towards utility. In the end it boils down to lack of money. And this is why the industry will focus on drugs that promise high revenues, regardless of impact on public health.

The things people know... Meanwhile : http://www.scienceforums.net/forum/showthread.php?t=52115 http://www.scienceforums.net/forum/showthread.php?t=52117 Mind you, artificial cells can also be lipid enclosures with a few proteins in it. This is not anywhere near a real cell, of course.

I am not quite sure what you try to achieve, but if genomic sequences are available for your species of interest and you know the gene (and by extension, the position in the genome of the relative gene) you can extract the respective up-and downstream region of each species and align them. I would go for multiple sequence alignments (e.g. clustalw) in order to see similiarities/dissimilarties between the respective loci.

Species do not modify themselves (in some cases they enhance mutation rates, but that is about the scope of it). In the simplest scenario variation exist and the most advantageous traits manage to propagate. In case of dog breeds however, generally artificial selection is prevalent. I.e. the breeder chooses what traits he likes and allow those to propagate, regardless whether the trait allows is connected to reproductive success in natural context or not. Under natural selection conditions only traits are selected that allow for an advantage in terms of propagation.

Most likely you saw Craig Venter's experiments. There is a thread about it somewhere here, but to summarize, it is was merely a large scale implementation of existing technologies, none of which are able to create custom organisms. What has been possible for decades is to manipulate organisms, however it is still a far shot from doing anything but the simplest manipulations (e.g. inserting genes that do not alter the existing organism too much or toying around with existing genes). We are still a far shot off of to e.g. engineer complex pathways and most attempts into manipulating simpler pathways often still yield unexpected results. This mostly due to the redundancy and flexibility of the underlying regulatory networks.

This is one possibility, yes. One could also directly measure metabolites. Of course, in earlier days you were a bit stuck with single compounds, but nowadays you could screen the whole metabolome.

Cool things about the spy ring Intelligence agencies need better script writers.

Think about what a phenotype is. Now think about a bacterium that is not able to utilize fatty acid as nutrient. Then imagine one that is auxotrophic for certain fatty acids. Now think about a bacterium that overaccumulates a certain amino acid. Now put that back into context of phenotypes.

How are metabolic changes not phenotypes?

15 k would be ridiculous. Average of over 30k sounds more reasonable. It is telling however that postdoc researchers make less money, although they work more hours. But then academia payrolls are ridiculous anyway.

This clearly limits the possibilities. Without the genomics info one is generally limited to reverse genetics techniques (you may want to look them up). Also I would ask myself the question under which conditions are the genes expressed and how are they controlled.

This is incorrect. Even the simplest model would include selective sweeps. No model is based on mutation alone as it would amount to no net change but merely fluctuations in a population. Moreover, even closely related species can inhabit different niches that put different constraints on genome size. He assumed that changes are gradual due to random accumulation of mutations. He followed that due to that closely related species should similar genomic contents, including size. However this would exclude selective forces, one of the basic mechanisms of evolution. While the sequences of closely related organism would be similar (due to phylogentic relationship) selective forces can rapidly change the overall shape of the genome in terms of gene losses or duplications, depending on the presence or absence of given constraints. In higher organized organisms the rate tends to be a bit lower as dramatic changes strongly affects e.g. their body development. Single celled organisms on the other hand can allow for more flexibility in terms of changes (and still survive it), but they often live under energetically limited conditions and smaller genome sizes can allow for faster propagation, for instance. And don't let me get started regarding horizontal gene transfer. It has also to be noted that Darwin's model is obviously not the current one. What has survived the test of time are certain elements regarding the inheritance and variance of traits (now pinned down to genes and mutations) as well as the shaping forces of natural selection (though much more has added to the mix). Also Darwin's model was qualitative whereas current ones are quantitative (if sufficient data is available).

Ah, you meant old samples that have not yet degraded? There is little. A bit is discussed in another thread but paleogenomics is very challenging and there is little that has survived which is still intact enough to sequence. Even if one should find frozen samples most of the time one will only get fragments.

What do you mean with degraded? There are species to species variatios, of course. The amount of genes they carry depends whether they live under constriction for genome size and the environmental conditions they live in. In protozoa the largest amount of genes have been found so far (around 60k, whereas humans are around 20-22k). In case you were wondering, complexity of organism does not scale with genome size, either. As a rule of thumb single celled organisms have to be much more flexible in terms of metabolic capabilities than more multicellular ones and require in relative terms a higher number of genes to respond accordingly. Exceptions are parasitic organisms, for instance that, similar to individual cells in our body, live in a relatively stable environment and hence are able to get by with less genes. In other words, environmental constraints generally play a bigger role in determining genome size as well as number of genes. Again, there is no evolutionary scaling in terms of genome size. A plot of species vs. number of genes would be all over the place, precisely as we would expect under standard evolutionary models.

Assessing the amount of genes in ancestors is not possible as most DNA is too degraded to get that information. Mammoth DNA was pretty bad to get already and in evolutionary terms that was just recently. That being said there is little evidence that there should be a correlation. Maybe in the very early days after life arose there may have been less diversity. But then rapid duplication events and similar will lead to a sudden increase of genes with selective sweeps eliminating them. The argument is based a often propagated fallacy that evolution should lead to an increase in genetic information. It does not. Also keep in mind that going back in evolution does not mean moving horizontally among extant species (e.g. from mammals to fishes) but back in time along the now extinct species.

I think you misunderstand why the US is in Afghanistan.

A lot of stuff is fluorescent. But that is not where the usefulness of the GFP comes in. Think about the uses of GFP and now try to but that into context of pyverdine synthesis.

Your decision is wrong. Pyoverdine is very different from GFP. It isn't even a protein and thus unsuited for basically all kind of experiments in which GFP is used. You have to read more carefully before coming to any conclusions.

Also, from what I understand he was instrumental in devising the strategy to begin with. Thus he is unlikely to criticize himself.