KESKUSTELU

Lisäksi richard dawkins loi ja julkitoi meemin, käsitteen meemi, joka tarkoittaa kulttuurigeeniä, replikaattoria, joka kopioi itsensä darwinistisesti.

Väitetään tosin, että geenien evoluutio darwinistista, mutta meemien ja teemien tai qumeemien (teemi=teknologinen meemi kuten esim. Kännykkä. qumeemi=kvanttimekaaninen meemi, sanasta quantum meme) evoluutio lamarckilaista. Google kertoo enemmän...

On selkeämpiä todisteita löytynyt Ruosin Överkalixista. Jokaisessa geenissä on DNA:n lisäksi eräänlainen on/off-kytkin, joka määrää otetaanko geeniä ollenkaan huomioon. Tätä kutsutaan epigenetiikaksi, epi on latinaa ja tarkoittaa edellä olevaa. Jos tuo geenin kytkin vaurioituu esimerkiksi nälkäkuoleman partaalla käydessä niin tuo vaurio, toisin kuin DNA, periytyy seuraavaan sukupolveen.

Tästä siis seuraa, että hankitut ominaisuudet jossain määrin periytyvät eli evoluutio on lamarckilaista.

Yläkaliksilla länsinaapurissa on pidetty tarkkoja tilastoja ja kirkonkirjoja karuissa oloissa kauan ja ainoa popperilaista epistemologiaa noudattava selitys todella on tuo 1800-luvun loppupuolen ylivoimaisesti aikalaistensa keskuudessa tunnetuimman, ensimmäisenä filosofina miljoona kirjaa myyneen Herbert Spencerin (hyshys) käsitys opittujen kykyjen osittaisesta periytymisestä.

Rewriting Darwin: The new non-genetic inheritance

* 09 July 2008
* From New Scientist
* Emma Young

http://groups.google.com/group/soc.cult ... 2969990515

HALF a century before Charles Darwin published On the Origin of
Species, the French naturalist Jean-Baptiste Lamarck outlined his own theory of evolution. A cornerstone of this was the idea that
characteristics acquired during an individual's lifetime can be passed on to their offspring. In its day, Lamarck's theory was generally ignored or lampooned. Then came Darwin, and Gregor Mendel's discovery of genetics.

In recent years, ideas along the lines of Richard Dawkins's concept of the "selfish gene" have come to dominate discussions about heritability, and with the exception of a brief surge of interest in the late 19th and early 20th centuries, "Lamarckism" has long been consigned to the theory junkyard.

Now all that is changing. No one is arguing that Lamarck got
everything right, but over the past decade it has become increasingly clear that environmental factors, such as diet or stress, can have biological consequences that are transmitted to offspring without a single change to gene sequences taking place. In fact, some biologists are already starting to consider this process as routine.

However, fully accepting the idea, provocatively dubbed the "new Lamarckism", would mean a radical rewrite of modern evolutionary theory. Not surprisingly, there are some who see that as heresy. "It means the demise of the selfish-gene theory," says Eva Jablonka at Tel Aviv University, Israel. "The whole discourse about heredity and evolution will change" (see "Rewriting Darwin and Dawkins?").

That's not all. The implications for public health could also be
immense. Some researchers are talking about a paradigm shift in
understanding the causes of disease. For example, non-genetic
inheritance might help explain the current obesity epidemic, or why there are family patterns for certain cancers and other disorders, but no discernible genetic cause. "It's a whole new way of looking at the inheritance and causes of various diseases, including schizophrenia, bipolar disorder and diabetes, as well as cancer," says Robyn Ward of the cancer research centre at the University of New South Wales in Sydney, Australia.

Lamarck's ideas about exactly how non-genetic inheritance might work were woolly at best. He wrote, for example, of the giraffe's neck becoming elongated over generations because of the animal's habit of stretching up to feed on leaves in high treetops. The recent research, by contrast, has a firm basis in biological mechanisms - in so-called "epigenetic" change.

Epigenetics deals with how gene activity is regulated within a cell -
which genes are switched on or off, which are dimmed and how, and when all this happens. For instance, while the cells in the liver and skin of an individual contain exactly the same DNA, their specific epigenetic settings mean the tissues look very different and do a totally different job. Likewise, different genes may be expressed in the same tissue at different stages of development and throughout life. Researchers are a long way from knowing exactly what mechanisms control all this, but they have made some headway.

Inside the nucleus, DNA is packaged around bundles of proteins called histones, which have tails that stick out from the core. One factor that affects gene expression is the pattern of chemical modifications to these tails, such as the presence or absence of acetyl and methyl groups. Genes can also be silenced directly via enzymes that bind methyl groups onto the DNA. The so-called RNA interference (RNAi) system can direct this activity, via small RNA strands. As well as controlling DNA methylation and modifying histones, these RNAi molecules target messenger RNA - much longer strands that act as intermediaries between DNA sequences and the proteins they code for.
By breaking mRNA down into small segments, the RNAi molecules ensure that a certain gene cannot be translated into its protein. In short, RNAi creates the epigenetic "marks" that control the activity of genes.

We know that genes - and possibly also non-coding DNA - control RNAi and so are involved in determining an individual's epigenetic
settings. It is becoming increasingly apparent, though, that
environmental factors can have a direct impact too, with potentially life-changing implications. The clearest example of this comes from honeybees. All female honeybees develop from genetically identical larvae, but those fed on royal jelly become fertile queens while the rest are doomed to life as sterile workers. In March this year, an Australian team led by Ryszard Maleszka at the Australian National University in Canberra showed that epigenetic mechanisms account for this. They used RNAi to silence a gene for DNA methyltransferase - an
enzyme necessary for adding methyl groups to DNA - in honeybee larvae. Most of these larvae emerged as queens, without ever having tasted royal jelly (Science, DOI: 10.1126/science.1153069).

“All female honeybees, including queens, develop from genetically
identical larvae”

For honeybees then, what they eat during early development creates an epigenetic setting that has fundamental lifelong implications. This is an extreme example, but researchers are starting to realise that similar mechanisms are at play in other animals, and even in humans.

And, as for honeybees, it seems there is a critical early period
during which an individual's pattern of gene expression is
"programmed" to a large extent. Environmental factors can feed into this programming, possibly with long-term health impacts.

In 2000, Randy Jirtle at Duke University in Durham, North Carolina, led a ground-breaking experiment on a strain of genetically identical mice. These mice carried the agouti gene, which makes them fat and prone to diabetes and cancer. Jirtle and his student Robert Waterland gave one group of females a diet rich in methyl groups before conception and during pregnancy. They found that the offspring were very different to their parents - they were slim and lived to a ripe old age. Though the pups had inherited the damaging agouti gene, the methyl groups had attached to the gene and dimmed its expression.

Jirtle then tried supplementing the diets of pregnant agouti mice with genistein, an oestrogen-like chemical found in soya. The dose was designed to be comparable to the amount consumed by a person on a high- soya diet, which is associated with a reduced risk of cancer and less body fat. These mice were also more likely to give birth to slim, healthy offspring which had less chance of becoming obese in adulthood. This change was associated with increased methylation of six DNA base-pair sites involved in regulating activity of the agouti gene.

These and other animal studies strongly suggest that a pregnant woman's diet can affect her child's epigenetic marks. So perhaps it is not surprising that the effect of certain nutrients is being called into question. Folate, for example, is a potent methyl donor.

It is routinely recommended during pregnancy and added to cereal products in certain countries, including the US, because it reduces the risk of spinal tube defects if eaten around the time of conception. But Jirtle wonders whether it could also be inducing as-yet-unknown, damaging epigenetic effects.

The legacy of stress...

http://sandwalk.blogspot.com/2008/07/ep ... ntist.html

Alkuperäinen linkki:

http://www.newscientist.com/channel/lif ... tance.html

On selkeämpiä todisteita löytynyt Ruosin Överkalixista. Jokaisessa geenissä on DNA:n lisäksi eräänlainen on/off-kytkin, joka määrää otetaanko geeniä ollenkaan huomioon. Tätä kutsutaan epigenetiikaksi, epi on latinaa ja tarkoittaa edellä olevaa. Jos tuo geenin kytkin vaurioituu esimerkiksi nälkäkuoleman partaalla käydessä niin tuo vaurio, toisin kuin DNA, periytyy seuraavaan sukupolveen.

Tästä siis seuraa, että hankitut ominaisuudet jossain määrin periytyvät eli evoluutio on lamarckilaista.

Yläkaliksilla länsinaapurissa on pidetty tarkkoja tilastoja ja kirkonkirjoja karuissa oloissa kauan ja ainoa popperilaista epistemologiaa noudattava selitys todella on tuo 1800-luvun loppupuolen ylivoimaisesti aikalaistensa keskuudessa tunnetuimman, ensimmäisenä filosofina miljoona kirjaa myyneen Herbert Spencerin (hyshys) käsitys opittujen kykyjen osittaisesta periytymisestä.

Rewriting Darwin: The new non-genetic inheritance

* 09 July 2008
* From New Scientist
* Emma Young

http://groups.google.com/group/soc.cult ... 2969990515

HALF a century before Charles Darwin published On the Origin of
Species, the French naturalist Jean-Baptiste Lamarck outlined his own theory of evolution. A cornerstone of this was the idea that
characteristics acquired during an individual's lifetime can be passed on to their offspring. In its day, Lamarck's theory was generally ignored or lampooned. Then came Darwin, and Gregor Mendel's discovery of genetics.

In recent years, ideas along the lines of Richard Dawkins's concept of the "selfish gene" have come to dominate discussions about heritability, and with the exception of a brief surge of interest in the late 19th and early 20th centuries, "Lamarckism" has long been consigned to the theory junkyard.

Now all that is changing. No one is arguing that Lamarck got
everything right, but over the past decade it has become increasingly clear that environmental factors, such as diet or stress, can have biological consequences that are transmitted to offspring without a single change to gene sequences taking place. In fact, some biologists are already starting to consider this process as routine.

However, fully accepting the idea, provocatively dubbed the "new Lamarckism", would mean a radical rewrite of modern evolutionary theory. Not surprisingly, there are some who see that as heresy. "It means the demise of the selfish-gene theory," says Eva Jablonka at Tel Aviv University, Israel. "The whole discourse about heredity and evolution will change" (see "Rewriting Darwin and Dawkins?").

That's not all. The implications for public health could also be
immense. Some researchers are talking about a paradigm shift in
understanding the causes of disease. For example, non-genetic
inheritance might help explain the current obesity epidemic, or why there are family patterns for certain cancers and other disorders, but no discernible genetic cause. "It's a whole new way of looking at the inheritance and causes of various diseases, including schizophrenia, bipolar disorder and diabetes, as well as cancer," says Robyn Ward of the cancer research centre at the University of New South Wales in Sydney, Australia.

Lamarck's ideas about exactly how non-genetic inheritance might work were woolly at best. He wrote, for example, of the giraffe's neck becoming elongated over generations because of the animal's habit of stretching up to feed on leaves in high treetops. The recent research, by contrast, has a firm basis in biological mechanisms - in so-called "epigenetic" change.

Epigenetics deals with how gene activity is regulated within a cell -
which genes are switched on or off, which are dimmed and how, and when all this happens. For instance, while the cells in the liver and skin of an individual contain exactly the same DNA, their specific epigenetic settings mean the tissues look very different and do a totally different job. Likewise, different genes may be expressed in the same tissue at different stages of development and throughout life. Researchers are a long way from knowing exactly what mechanisms control all this, but they have made some headway.

Inside the nucleus, DNA is packaged around bundles of proteins called histones, which have tails that stick out from the core. One factor that affects gene expression is the pattern of chemical modifications to these tails, such as the presence or absence of acetyl and methyl groups. Genes can also be silenced directly via enzymes that bind methyl groups onto the DNA. The so-called RNA interference (RNAi) system can direct this activity, via small RNA strands. As well as controlling DNA methylation and modifying histones, these RNAi molecules target messenger RNA - much longer strands that act as intermediaries between DNA sequences and the proteins they code for.
By breaking mRNA down into small segments, the RNAi molecules ensure that a certain gene cannot be translated into its protein. In short, RNAi creates the epigenetic "marks" that control the activity of genes.

We know that genes - and possibly also non-coding DNA - control RNAi and so are involved in determining an individual's epigenetic
settings. It is becoming increasingly apparent, though, that
environmental factors can have a direct impact too, with potentially life-changing implications. The clearest example of this comes from honeybees. All female honeybees develop from genetically identical larvae, but those fed on royal jelly become fertile queens while the rest are doomed to life as sterile workers. In March this year, an Australian team led by Ryszard Maleszka at the Australian National University in Canberra showed that epigenetic mechanisms account for this. They used RNAi to silence a gene for DNA methyltransferase - an
enzyme necessary for adding methyl groups to DNA - in honeybee larvae. Most of these larvae emerged as queens, without ever having tasted royal jelly (Science, DOI: 10.1126/science.1153069).

“All female honeybees, including queens, develop from genetically
identical larvae”

For honeybees then, what they eat during early development creates an epigenetic setting that has fundamental lifelong implications. This is an extreme example, but researchers are starting to realise that similar mechanisms are at play in other animals, and even in humans.

And, as for honeybees, it seems there is a critical early period
during which an individual's pattern of gene expression is
"programmed" to a large extent. Environmental factors can feed into this programming, possibly with long-term health impacts.

In 2000, Randy Jirtle at Duke University in Durham, North Carolina, led a ground-breaking experiment on a strain of genetically identical mice. These mice carried the agouti gene, which makes them fat and prone to diabetes and cancer. Jirtle and his student Robert Waterland gave one group of females a diet rich in methyl groups before conception and during pregnancy. They found that the offspring were very different to their parents - they were slim and lived to a ripe old age. Though the pups had inherited the damaging agouti gene, the methyl groups had attached to the gene and dimmed its expression.

Jirtle then tried supplementing the diets of pregnant agouti mice with genistein, an oestrogen-like chemical found in soya. The dose was designed to be comparable to the amount consumed by a person on a high- soya diet, which is associated with a reduced risk of cancer and less body fat. These mice were also more likely to give birth to slim, healthy offspring which had less chance of becoming obese in adulthood. This change was associated with increased methylation of six DNA base-pair sites involved in regulating activity of the agouti gene.

These and other animal studies strongly suggest that a pregnant woman's diet can affect her child's epigenetic marks. So perhaps it is not surprising that the effect of certain nutrients is being called into question. Folate, for example, is a potent methyl donor.

It is routinely recommended during pregnancy and added to cereal products in certain countries, including the US, because it reduces the risk of spinal tube defects if eaten around the time of conception. But Jirtle wonders whether it could also be inducing as-yet-unknown, damaging epigenetic effects.

The legacy of stress...

http://sandwalk.blogspot.com/2008/07/ep ... ntist.html

Alkuperäinen linkki:

http://www.newscientist.com/channel/lif ... tance.html

Eipäs sekoiteta materialismia ja reduktionismia keskenään. Ne eivät ole toisiinsa sidottuja asioita.

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Arkielämän havainto: Jotkut linnut Englannissa ennen sotaa olivat oppineet avaamaan maitopullon kannen. Maitopullot katosivat katukuvasta sodan ajaksi. Kun ne taas ilmestyivät, osasivat em. lintujen jälkeläiset avata maitopullojen kannet. Mot?

Linnut, joilla on fyysiset edellytykset avata maitopulloja, elävät usein pidempään kuin mitä sota kesti. Lisäksi samalla tavalla ne voivat avata paljon muutakin.

Jos evoluutio toimisi, niin Damasion täytyisi olla hyvin varustettu.

Ei koolla ole väliä, vaan sillä miten varustuksia käyttää.