One person can have many DNAs,Chimerism,
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From biology class to CSI, we are told again and again that our genome
is at the heart of our identity. Read the sequences in the chromosomes
of a single cell, and learn everything about a person's genetic
information — or, as 23andme, a prominent genetic testing company, says
on its website, "The more you know about your DNA, the more you know
about yourself."
But scientists are discovering that — to a surprising degree — we contain genetic multitudes . Not long ago, researchers had thought it was rare for the cells in a single healthy person to differ genetically in a significant way. But scientists are finding that it's quite common for an individual to have multiple genomes. Some people, for example, have groups of cells with mutations that are not found in the rest of the body. Some have genomes that came from other people.
"There have been whispers in the matrix about this for years, even decades, but only in a very hypothetical sense," said Alexander Urban, a geneticist at Stanford University. Even three years ago, suggesting that there was widespread genetic variation in a single body would have been met with scepticism, he said. "You would have just run against the wall." But a series of recent papers by Dr Urban and others has demonstrated that those whispers were not just hypothetical. The variation in the genomes found in a single person is too large to be ignored. "We now know it's there," Dr Urban said. "Now we're mapping this new continent."
Science's changing view is also raising questions about how forensic scientists should use DNA evidence to identify people. It's also posing challenges for genetic counsellors, who can't assume that the genetic information from one cell can tell them about the DNA throughout a person's body.
The cost of sequencing an entire genome has fallen so drastically in the past 20 years — now a few thousand dollars, down from an estimated $3 billion for the public-private partnership that sequenced the first human genome — that doctors are beginning to sequence the entire genomes of some patients. (Sequencing can be done in as little as 50 hours.) And they're identifying links between mutations and diseases that have never been seen before.
Yet all these powerful tests are based on the assumption that, inside our body, a genome is a genome is a genome. Scientists believed that they could look at the genome from cells taken in a cheek swab and be able to learn about the genomes of cells in the brain or the liver or anywhere else in the body.
In the mid-1900 s, scientists began to get clues that this was not always true. In 1953, for example, a British woman donated a pint of blood. It turned out that some of her blood was Type O and some was Type A. The scientists who studied her concluded that she had acquired some of her blood from her twin brother in the womb, including his genomes in his blood cells.
Chimerism, as such conditions came to be known, seemed for many years to be a rarity. But "it can be commoner than we realized ," said Dr Linda Randolph, a pediatrician at Children's Hospital in Los Angeles who is an author of a review of chimerism published in The American Journal of Medical Genetics in July.
Twins can end up with a mixed supply of blood when they get nutrients in the womb through the same set of blood vessels . In other cases, two fertilized eggs may fuse together. These socalled embryonic chimeras may go through life blissfully unaware of their origins.
Women can also gain genomes from their children. After a baby is born, it may leave some fetal cells behind in its mother's body, where they can travel to different organs and be absorbed into those tissues. "It's pretty likely that any woman who has been pregnant is a chimera," Dr Randolph said.
But scientists are discovering that — to a surprising degree — we contain genetic multitudes . Not long ago, researchers had thought it was rare for the cells in a single healthy person to differ genetically in a significant way. But scientists are finding that it's quite common for an individual to have multiple genomes. Some people, for example, have groups of cells with mutations that are not found in the rest of the body. Some have genomes that came from other people.
"There have been whispers in the matrix about this for years, even decades, but only in a very hypothetical sense," said Alexander Urban, a geneticist at Stanford University. Even three years ago, suggesting that there was widespread genetic variation in a single body would have been met with scepticism, he said. "You would have just run against the wall." But a series of recent papers by Dr Urban and others has demonstrated that those whispers were not just hypothetical. The variation in the genomes found in a single person is too large to be ignored. "We now know it's there," Dr Urban said. "Now we're mapping this new continent."
Science's changing view is also raising questions about how forensic scientists should use DNA evidence to identify people. It's also posing challenges for genetic counsellors, who can't assume that the genetic information from one cell can tell them about the DNA throughout a person's body.
The cost of sequencing an entire genome has fallen so drastically in the past 20 years — now a few thousand dollars, down from an estimated $3 billion for the public-private partnership that sequenced the first human genome — that doctors are beginning to sequence the entire genomes of some patients. (Sequencing can be done in as little as 50 hours.) And they're identifying links between mutations and diseases that have never been seen before.
Yet all these powerful tests are based on the assumption that, inside our body, a genome is a genome is a genome. Scientists believed that they could look at the genome from cells taken in a cheek swab and be able to learn about the genomes of cells in the brain or the liver or anywhere else in the body.
In the mid-1900 s, scientists began to get clues that this was not always true. In 1953, for example, a British woman donated a pint of blood. It turned out that some of her blood was Type O and some was Type A. The scientists who studied her concluded that she had acquired some of her blood from her twin brother in the womb, including his genomes in his blood cells.
Chimerism, as such conditions came to be known, seemed for many years to be a rarity. But "it can be commoner than we realized ," said Dr Linda Randolph, a pediatrician at Children's Hospital in Los Angeles who is an author of a review of chimerism published in The American Journal of Medical Genetics in July.
Twins can end up with a mixed supply of blood when they get nutrients in the womb through the same set of blood vessels . In other cases, two fertilized eggs may fuse together. These socalled embryonic chimeras may go through life blissfully unaware of their origins.
Women can also gain genomes from their children. After a baby is born, it may leave some fetal cells behind in its mother's body, where they can travel to different organs and be absorbed into those tissues. "It's pretty likely that any woman who has been pregnant is a chimera," Dr Randolph said.
Switch controlling growth of aggressive brain tumour cells identified
WASHINGTON:
Researchers have identified a cellular switch that can be turned off
and on, to slow down, and eventually restrict the growth of the most
commonly diagnosed and aggressive malignant brain tumour.
The findings show that the protein RIP1 acts as a mediator of brain tumor cell survival, either protecting or destroying cells.
According to the researchers the protein, found in most glioblastomas, can be targeted to develop a drug treatment for these highly malignant brain tumors.
Senior author Dr Amyn Habib, associate professor of neurology and neurotherapeutics at UT Southwestern Medical Center, said that their study identifies a new mechanism involving RIP1that regulates cell division and death in glioblastomas.
She said that for individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist.
In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NFkB, a family of proteins that is important to the growth of cancerous tumor cells. When RIP1 is switched off in the experimental model, NFkB and the signalling that promotes tumour growth is also inhibited. Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.
The study has been published online in Cell Reports.
The findings show that the protein RIP1 acts as a mediator of brain tumor cell survival, either protecting or destroying cells.
According to the researchers the protein, found in most glioblastomas, can be targeted to develop a drug treatment for these highly malignant brain tumors.
Senior author Dr Amyn Habib, associate professor of neurology and neurotherapeutics at UT Southwestern Medical Center, said that their study identifies a new mechanism involving RIP1that regulates cell division and death in glioblastomas.
She said that for individuals with glioblastomas, this finding identified a target for the development of a drug treatment option that currently does not exist.
In the study, researchers used animal models to examine the interactions of the cell receptor EGFRvIII and RIP1. Both are used to activate NFkB, a family of proteins that is important to the growth of cancerous tumor cells. When RIP1 is switched off in the experimental model, NFkB and the signalling that promotes tumour growth is also inhibited. Furthermore, the findings show that RIP1 can be activated to divert cancer cells into a death mode so that they self-destruct.
The study has been published online in Cell Reports.
Protein that can mean life or death for cells identified
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LONDON: Scientists have identified a protein that plays a crucial role in correctly measuring stress levels, and also makes sure the pathways of cell repair or cell death in the body are effective.
Each cell in an organism has a sensor that measures the health of its "internal" environment, researchers said.
This "alarm" is found in the endoplasmic reticulum (ER), which is able to sense cellular stress and trigger either rescue responses or the death of the cell.
A team from the Institute for Research in Biomedicine (IRB), in Barcelona, found some of the molecular mechanisms that connect the protein Mitofusin 2 (Mfn2) to endoplasmic reticulum stress.
When the scientists removed Mfn2 from the cell under conditions of cell stress, the endoplasmic reticulum responded by over-activating the repair pathways.
By doing so, it contradictorily functioned worse, reducing the capacity of cells to overcome the stress insult and promoting to a lesser degree apoptotic cell death.
"When Mfn2 is removed, the cellular stress response pathways are completely disrupted," said Antonio Zorzano, coordinator of IRB's Molecular Medicine Programme.
The study investigated the relationship between mitochondria and the endoplasmic reticulum, and indicated that changes in mitochondria, caused by the loss of the Mfn2 protein, directly affect the endoplasmic reticulum function.
"We have shown that Mfn2 is important for cell viability and has implications for numerous diseases, such as neurodegeration, cancer, cardiovascular disease, in addition to diabetes," said postdoctoral researcher Juan Pablo Munoz, first author of the study.
"The fact that we can modulate cell damage response with Mfn2 opens a wide window of possible therapeutic avenues for further study," said Munoz.
Munoz explained that tumour cells don't activate cell death properly and proliferate uncontrolled.
"Cancer cells have already been noted to have low Mfn2 levels, and if we could increase such levels, we would be able to promote apoptosis," Munoz said.
Each cell in an organism has a sensor that measures the health of its "internal" environment, researchers said.
This "alarm" is found in the endoplasmic reticulum (ER), which is able to sense cellular stress and trigger either rescue responses or the death of the cell.
A team from the Institute for Research in Biomedicine (IRB), in Barcelona, found some of the molecular mechanisms that connect the protein Mitofusin 2 (Mfn2) to endoplasmic reticulum stress.
When the scientists removed Mfn2 from the cell under conditions of cell stress, the endoplasmic reticulum responded by over-activating the repair pathways.
By doing so, it contradictorily functioned worse, reducing the capacity of cells to overcome the stress insult and promoting to a lesser degree apoptotic cell death.
"When Mfn2 is removed, the cellular stress response pathways are completely disrupted," said Antonio Zorzano, coordinator of IRB's Molecular Medicine Programme.
The study investigated the relationship between mitochondria and the endoplasmic reticulum, and indicated that changes in mitochondria, caused by the loss of the Mfn2 protein, directly affect the endoplasmic reticulum function.
"We have shown that Mfn2 is important for cell viability and has implications for numerous diseases, such as neurodegeration, cancer, cardiovascular disease, in addition to diabetes," said postdoctoral researcher Juan Pablo Munoz, first author of the study.
"The fact that we can modulate cell damage response with Mfn2 opens a wide window of possible therapeutic avenues for further study," said Munoz.
Munoz explained that tumour cells don't activate cell death properly and proliferate uncontrolled.
"Cancer cells have already been noted to have low Mfn2 levels, and if we could increase such levels, we would be able to promote apoptosis," Munoz said.
Nice guys and girls are sexier
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Helping others doesn't just make you feel good about yourself — it also increases your chances of having sex, a study has revealed.
Altruistic acts of kindness, from helping the elderly cross the road to donating bone marrow, made hypothetical objects of affection more sexually attractive to men and women in an experiment run by the University of Nottingham.
Scientists analysed the responses of 32 heterosexual women and 35 heterosexual men who were asked to rate how attractive they found a prospective partner based on a given list of known behaviours, characteristics and activities.
Working in collaboration with the Liverpool John Moores University, researchers found that both sexes rated someone as more attractive for a potential long-term relationship if they exhibited selflessness — though nice guys appeared to benefit more than nice girls.
While evolutionary biologists anticipated this outcome — with altruism identified as both a positive genetic and non-genetic trait for bringing up children — what was surprising was the fact that the same applied even when the proposed "relationship " would be a short-term fling.
When asked how attractive they found someone for a brief sexual encounter with little chance of conception , women were still drawn to men who exhibited selflessness. The same was less true, however, for men.
Dr Freya Harrison, a research fellow at The University of Nottingham's Life Sciences Centre for Biomolecular Sciences and senior author of the report, said: "We're not sure whether being helpful to others signals that you're more likely to be a good parent or whether it might be a signal that you carry 'good genes' that will produce healthy children — having the energy and ability to help others might be a show of vigour, rather like a peacock's tail."
Altruistic acts of kindness, from helping the elderly cross the road to donating bone marrow, made hypothetical objects of affection more sexually attractive to men and women in an experiment run by the University of Nottingham.
Scientists analysed the responses of 32 heterosexual women and 35 heterosexual men who were asked to rate how attractive they found a prospective partner based on a given list of known behaviours, characteristics and activities.
Working in collaboration with the Liverpool John Moores University, researchers found that both sexes rated someone as more attractive for a potential long-term relationship if they exhibited selflessness — though nice guys appeared to benefit more than nice girls.
While evolutionary biologists anticipated this outcome — with altruism identified as both a positive genetic and non-genetic trait for bringing up children — what was surprising was the fact that the same applied even when the proposed "relationship " would be a short-term fling.
When asked how attractive they found someone for a brief sexual encounter with little chance of conception , women were still drawn to men who exhibited selflessness. The same was less true, however, for men.
Dr Freya Harrison, a research fellow at The University of Nottingham's Life Sciences Centre for Biomolecular Sciences and senior author of the report, said: "We're not sure whether being helpful to others signals that you're more likely to be a good parent or whether it might be a signal that you carry 'good genes' that will produce healthy children — having the energy and ability to help others might be a show of vigour, rather like a peacock's tail."
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