I found these two statements in the article to be somewhat at odds with each other.
1. "The viruses that we found are very old, are integrated in the bird genome, and do not have the potential to encode any functional protein product," said Dr Gilbert. "So they do not have any effect in songbirds."
2. "a strikingly slow, long-term mutation rate that is 1,000 times slower than the viral [mutation] rates that had previously been estimated based on comparisons of currently circulating viral sequences only."
If the sequences are being in someway preserved they may well be having an effect. Perhaps not coding a protein themselves but altering the levels, timing or tissue specificity of gene expression in their vicinity. Also the presence of these similar sequences throughout the songbird genome can drive novel DNA recombination events which can result in new phenotypes, driving songbird evolution.
Interesting to look at the HapMap. You should feel very safe if your driver is of sub saharan African descent. They don't seem to have the minor allele at all
http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?rs=6265#Diversity . Of course one allele rarely controls the whole show.
As for solar energy, Australia has so much sunlight we'd have to be crazy not to make use of it. I know there are problems with transmission if you put a big solar plant out in the middle of nowhere, but that's not what I'm talking about. Think about all of the roofs in all of the cities - not just residential, either. How much solar energy is being wasted just bouncing off of the corrugated iron roofs of warehouses and factories? Put solar collectors on them, and they'd probably generate more power than they'd use - at least during the day, and most factories shut down at night.
I like the cut of your jib. Furthermore I will happily rent out my North facing roof space (Adelaide, South Australia) to first power company that wants to install solar panels on it. I looked into doing this myself but it is not an economically viable option for an individual household at present and I am too mean spirited just to do it for the dolphins.
Not really, DNA is just a salt by itself it is not really dangerous. Consider if you have eaten anything that was at some point a living object (such as a steak or piece of fruit or a vegetable). That stuff is full of DNA and it hasn't killed you yet.
I am surprised that the forensics lab that has been doing this testing did not run the appropriate negative control (cotton swab only) in their PCRs. DNA evidence alone would not lead to a conviction especially if this woman has alibis for the times these crimes were committed (such as she was busy packing cotton swabs at the time of the murder).
The inheritance mechanism is interesting but for practical purposes is not necessary to understand to start applying this knowledge. This holds great promise for those who suffer from neurological disorders where there appears to be both a genetic and environmental component to the phenotype (eg. bipolar). An equivalent "enriched" environment (eg. improved socio-economic conditions, tailored primary education programmes, etc. rather than say institutionalisation) might help families with a history of these disorders reduce the severity of symptoms over successive generations.
Actually you are kind of correct there. For the X chromosome at least. Women carrying two copies of the X chromosome, one of which has a novel mutation will "test" that mutation in all of her sons that get that mutation (biology 101: Human males will only get one X chromosome from their mother). The mutation will either be tolerated (and may confer some small advantage) or not tolerated (result in death). Therefore to a certain extent women drive evolution at a molecular level.
It is a common mistake to think that the evolution of a biological organism proceeds in a logical fashion. Mutations in DNA occur at random, the mutation is either tolerated or not tolerated. If it is not tolerated you die, if it is tolerated you get along fine. Maybe with your two organism example under certain circumstances having a less efficient encoding might put you at an advantage. Maybe being too efficient uses up your resources too quickly. Maybe if you rely on your one super efficient gene to get you through life you will be dead when it gets a mutation in it.
There are plenty of examples of of genes that appear to be almost entirely redundant. Many biologists will be able to tell you how they knocked their very important gene out of a mouse only to discover that the mouse survives will no ill effects. A lot of research goes into redundancy of genes. If you have a disease caused by a mutation in gene X which can be rescued by activating gene Y which serves a redundant function then that is going to put you at an advantage.
Perhaps I have missed your point for your third comment but; The obsession with zeroing in on the magic gene that causes X can be answered for you by anyone who has type I diabetes, or indeed any other monogenic disorder that has been treated following the discovery of the gene that causes the disease. Polygenic disorders are not a novel concept however we know less about them because it turns out that it is rather difficult to find out which variants of which genes are contributing to a disorder. If you like to donate to the complete sequencing of every human on the planet which would be the best way to solve this problem, I am sure someone will be willing to take you money.
Muscles do contract lengthwise but the force at the molecular level is driven by a lever arm, namley myosin. As such, all of the muscle filaments stay the same length and do not contract merely "slide" over each other.
A single gene can encode for multiple proteins through the use of alternate start sites for RNA transcription or the use of alternatively spliced exons. This would be the case for most of the coding genes in the human genome. I would suggest however, that gene a encodes for thousands or even hundreds of different proteins would be extremely rare.
That said, I agree that there are many ways to modify the activity of a particular protein and also the 3-D structure. Post-translational modifications such as phosphorylation, methylation and glycosylation for example.
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I found these two statements in the article to be somewhat at odds with each other.
1. "The viruses that we found are very old, are integrated in the bird genome, and do not have the potential to encode any functional protein product," said Dr Gilbert. "So they do not have any effect in songbirds."
2. "a strikingly slow, long-term mutation rate that is 1,000 times slower than the viral [mutation] rates that had previously been estimated based on comparisons of currently circulating viral sequences only."
If the sequences are being in someway preserved they may well be having an effect. Perhaps not coding a protein themselves but altering the levels, timing or tissue specificity of gene expression in their vicinity. Also the presence of these similar sequences throughout the songbird genome can drive novel DNA recombination events which can result in new phenotypes, driving songbird evolution.
Interesting to look at the HapMap. You should feel very safe if your driver is of sub saharan African descent. They don't seem to have the minor allele at all http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?rs=6265#Diversity . Of course one allele rarely controls the whole show.
and just waste whatever is left over after that
As for solar energy, Australia has so much sunlight we'd have to be crazy not to make use of it. I know there are problems with transmission if you put a big solar plant out in the middle of nowhere, but that's not what I'm talking about. Think about all of the roofs in all of the cities - not just residential, either. How much solar energy is being wasted just bouncing off of the corrugated iron roofs of warehouses and factories? Put solar collectors on them, and they'd probably generate more power than they'd use - at least during the day, and most factories shut down at night.
I like the cut of your jib. Furthermore I will happily rent out my North facing roof space (Adelaide, South Australia) to first power company that wants to install solar panels on it. I looked into doing this myself but it is not an economically viable option for an individual household at present and I am too mean spirited just to do it for the dolphins.
Not really, DNA is just a salt by itself it is not really dangerous. Consider if you have eaten anything that was at some point a living object (such as a steak or piece of fruit or a vegetable). That stuff is full of DNA and it hasn't killed you yet. I am surprised that the forensics lab that has been doing this testing did not run the appropriate negative control (cotton swab only) in their PCRs. DNA evidence alone would not lead to a conviction especially if this woman has alibis for the times these crimes were committed (such as she was busy packing cotton swabs at the time of the murder).
The inheritance mechanism is interesting but for practical purposes is not necessary to understand to start applying this knowledge. This holds great promise for those who suffer from neurological disorders where there appears to be both a genetic and environmental component to the phenotype (eg. bipolar). An equivalent "enriched" environment (eg. improved socio-economic conditions, tailored primary education programmes, etc. rather than say institutionalisation) might help families with a history of these disorders reduce the severity of symptoms over successive generations.
Actually you are kind of correct there. For the X chromosome at least. Women carrying two copies of the X chromosome, one of which has a novel mutation will "test" that mutation in all of her sons that get that mutation (biology 101: Human males will only get one X chromosome from their mother). The mutation will either be tolerated (and may confer some small advantage) or not tolerated (result in death). Therefore to a certain extent women drive evolution at a molecular level.
It is a common mistake to think that the evolution of a biological organism proceeds in a logical fashion. Mutations in DNA occur at random, the mutation is either tolerated or not tolerated. If it is not tolerated you die, if it is tolerated you get along fine. Maybe with your two organism example under certain circumstances having a less efficient encoding might put you at an advantage. Maybe being too efficient uses up your resources too quickly. Maybe if you rely on your one super efficient gene to get you through life you will be dead when it gets a mutation in it.
There are plenty of examples of of genes that appear to be almost entirely redundant. Many biologists will be able to tell you how they knocked their very important gene out of a mouse only to discover that the mouse survives will no ill effects. A lot of research goes into redundancy of genes. If you have a disease caused by a mutation in gene X which can be rescued by activating gene Y which serves a redundant function then that is going to put you at an advantage.
Perhaps I have missed your point for your third comment but; The obsession with zeroing in on the magic gene that causes X can be answered for you by anyone who has type I diabetes, or indeed any other monogenic disorder that has been treated following the discovery of the gene that causes the disease. Polygenic disorders are not a novel concept however we know less about them because it turns out that it is rather difficult to find out which variants of which genes are contributing to a disorder. If you like to donate to the complete sequencing of every human on the planet which would be the best way to solve this problem, I am sure someone will be willing to take you money.
If you have access to Science it looks like some of this work was published last October. I haven't read through it properley but the abstract looks like it is the same http://www.sciencemag.org/cgi/content/abstract/306 /5696/704
Muscles do contract lengthwise but the force at the molecular level is driven by a lever arm, namley myosin. As such, all of the muscle filaments stay the same length and do not contract merely "slide" over each other.
A single gene can encode for multiple proteins through the use of alternate start sites for RNA transcription or the use of alternatively spliced exons. This would be the case for most of the coding genes in the human genome. I would suggest however, that gene a encodes for thousands or even hundreds of different proteins would be extremely rare. That said, I agree that there are many ways to modify the activity of a particular protein and also the 3-D structure. Post-translational modifications such as phosphorylation, methylation and glycosylation for example.
won't that get in the way of it's ear? http://bioteach.ubc.ca/TeachingResources/Genetics/ Mouse&Ear.jpg