23 May 2013 Mutation Mapping To cure a disease you need to first understand its cause. Cancers come in all shapes and sizes, but genetic mutations – a few small changes in pivotal DNA sequences – play a role in almost every case. Acute myeloid leukaemia (AML) is an aggressive cancer of the blood that kills thousands of people worldwide each year. In a bid to understand what genes might be sparking the disease, scientists sequenced the genomes of over 200 AML patients, comparing the genetic sequences in their cancerous cells with those in their healthy cells. The result? A list of which genes and pathways contribute to the cancer. In this interactive graphic each dark line represents a single patient, connecting the mutations that appear in their cancer and revealing which mutations are most common. By identifying the genes that commonly cause the cancer, the researchers hope to dig up new ways to fight AML. Written by Anthony Lewis — Click here for the interactive graphic Ben Raphael Brown University, USA Research published in the New England Journal of Medicine
Pop-upView Separately
23 May 2013

Mutation Mapping

To cure a disease you need to first understand its cause. Cancers come in all shapes and sizes, but genetic mutations – a few small changes in pivotal DNA sequences – play a role in almost every case. Acute myeloid leukaemia (AML) is an aggressive cancer of the blood that kills thousands of people worldwide each year. In a bid to understand what genes might be sparking the disease, scientists sequenced the genomes of over 200 AML patients, comparing the genetic sequences in their cancerous cells with those in their healthy cells. The result? A list of which genes and pathways contribute to the cancer. In this interactive graphic each dark line represents a single patient, connecting the mutations that appear in their cancer and revealing which mutations are most common. By identifying the genes that commonly cause the cancer, the researchers hope to dig up new ways to fight AML.

Written by Anthony Lewis

—

Source: bpod.mrc.ac.uk

16 May 2013 Farm to Pharmacy Tobacco may soon shed its negative image by becoming a pharmaceutical factory. The disorganised blobs of tissue pictured, known as callus, will grow into genetically modified tobacco plants that can produce a therapeutic anti-HIV antibody. Molecular farming (also known as ‘pharming’) involves genetically modifying plants to produce medically useful proteins like antibodies, vaccines and hormones. Tobacco is ideal for pharming as it’s easy to grow and harvest, and as a non-food plant, there’s no chance of gene transfer into the food chain. The first small-scale clinical trials of the tobacco HIV antibody have shown it’s safe, and further testing will establish if it’s effective. ‘Plantibodies’ could revolutionise medical treatment, reducing costs dramatically, but concerns over the safety and ethics of large-scale production have slowed progress. If these trials are successful, perhaps greenhouses will become the drugs factories of the future. Written by Sarah McLusky — Originally published under a Creative Commons license (CC BY-SA 3.0, Igge)
Pop-upView Separately
16 May 2013

Farm to Pharmacy

Tobacco may soon shed its negative image by becoming a pharmaceutical factory. The disorganised blobs of tissue pictured, known as callus, will grow into genetically modified tobacco plants that can produce a therapeutic anti-HIV antibody. Molecular farming (also known as ‘pharming’) involves genetically modifying plants to produce medically useful proteins like antibodies, vaccines and hormones. Tobacco is ideal for pharming as it’s easy to grow and harvest, and as a non-food plant, there’s no chance of gene transfer into the food chain. The first small-scale clinical trials of the tobacco HIV antibody have shown it’s safe, and further testing will establish if it’s effective. ‘Plantibodies’ could revolutionise medical treatment, reducing costs dramatically, but concerns over the safety and ethics of large-scale production have slowed progress. If these trials are successful, perhaps greenhouses will become the drugs factories of the future.

Written by Sarah McLusky

—

  • Originally published under a Creative Commons license (CC BY-SA 3.0, Igge)
11 May 2013 Cancer Culprit Eye colour, body shape, whether we can roll our tongues: genes affect everything about us. These genetic programs carry within them the code needed to create proteins – the building blocks of life. Given this essential role, it is perhaps unsurprising that genes also play a major part in some diseases. With gastric cancer (a microscopic section pictured), the activity of one gene, called CAV-1, is particularly important. As tumour cells (orange) take hold, the gene becomes less and less active in producing proteins. Although this shift occurs throughout the tumour, it’s in its connective tissue (green) where this drop in work rate appears to have the greatest toll. Lower levels of CAV-1 activity in these areas predict higher rates of death and recurrence in patients. Therefore, targeting CAV-1 within the connective tissue of tumours may offer a good opportunity for fighting the disease. Written by Jan Piotrowski — Honglei Chen Wuhan University, China Originally published under a Creative Commons Attribution license Published in PLoS ONE 8(3): e59102
Pop-upView Separately
11 May 2013

Cancer Culprit

Eye colour, body shape, whether we can roll our tongues: genes affect everything about us. These genetic programs carry within them the code needed to create proteins – the building blocks of life. Given this essential role, it is perhaps unsurprising that genes also play a major part in some diseases. With gastric cancer (a microscopic section pictured), the activity of one gene, called CAV-1, is particularly important. As tumour cells (orange) take hold, the gene becomes less and less active in producing proteins. Although this shift occurs throughout the tumour, it’s in its connective tissue (green) where this drop in work rate appears to have the greatest toll. Lower levels of CAV-1 activity in these areas predict higher rates of death and recurrence in patients. Therefore, targeting CAV-1 within the connective tissue of tumours may offer a good opportunity for fighting the disease.

Written by Jan Piotrowski

—

26 April 2013 Roll-up, Zip-up The fun in science isn’t just about knowing things. It’s about the pleasure of finding things out. Although doing science can be drudgery sometimes, the pay-off can compare to the thrill of cracking a masterful crime. Few medical mysteries are harder to crack than those caused by the complicity between environmental factors and faulty genes, such as neural tube defects (NTDs) causing spina bifida when the spinal tube fails to roll-up and zip-up seamlessly (as in the amphibian NTs in the lower time-lapse images). Although pregnant women routinely take folic acid supplements to cut the likelihood of NTDs, newborns with the condition persist at 1/1000 in the developed world and several times higher elsewhere, making it one of the commonest birth defects. Genes are at the bottom of this – over 200 of them at the latest count. By a process of elimination, scientist-detectives are now painstakingly homing-in on the culprits. Written by Tristan Farrow — John Wallingford The University of Texas at Austin, USA Reprinted with permission from AAAS. Published in Science 339 (6123)
Pop-upView Separately
26 April 2013

Roll-up, Zip-up

The fun in science isn’t just about knowing things. It’s about the pleasure of finding things out. Although doing science can be drudgery sometimes, the pay-off can compare to the thrill of cracking a masterful crime. Few medical mysteries are harder to crack than those caused by the complicity between environmental factors and faulty genes, such as neural tube defects (NTDs) causing spina bifida when the spinal tube fails to roll-up and zip-up seamlessly (as in the amphibian NTs in the lower time-lapse images). Although pregnant women routinely take folic acid supplements to cut the likelihood of NTDs, newborns with the condition persist at 1/1000 in the developed world and several times higher elsewhere, making it one of the commonest birth defects. Genes are at the bottom of this – over 200 of them at the latest count. By a process of elimination, scientist-detectives are now painstakingly homing-in on the culprits.

Written by Tristan Farrow

—

23 April 2013 Enhancing Expression Multicellular organisms contain a cornucopia of different cell types. Each has specific characteristics and functions, even though almost all contain the same genetic information. Such diversity is possible because each cell type expresses a unique subset of the genes encoded in DNA, a process controlled by non-coding sections of the genome called enhancers. Researchers don’t know much about them yet, but have recently come up with a way to identify the DNA sequences that function as enhancers and measure their activity in specific cells. Pictured are fruit fly ovary cells used to validate the method, with DNA stained fluorescent blue, and green representing the strength of enhancer activity. Scientists hope to use the technique to map the regulatory parts of the human genome and study how they’re involved in turning genes on and off during normal development and disease. Written by Daniel Cossins — Arnold Cosmas Research Institute of Molecular Pathology, Austria Reprinted with permission from AAAS. Published in Science 339(6123): 1074-1077
Pop-upView Separately
23 April 2013

Enhancing Expression

Multicellular organisms contain a cornucopia of different cell types. Each has specific characteristics and functions, even though almost all contain the same genetic information. Such diversity is possible because each cell type expresses a unique subset of the genes encoded in DNA, a process controlled by non-coding sections of the genome called enhancers. Researchers don’t know much about them yet, but have recently come up with a way to identify the DNA sequences that function as enhancers and measure their activity in specific cells. Pictured are fruit fly ovary cells used to validate the method, with DNA stained fluorescent blue, and green representing the strength of enhancer activity. Scientists hope to use the technique to map the regulatory parts of the human genome and study how they’re involved in turning genes on and off during normal development and disease.

Written by Daniel Cossins

—

21 April 2013 Change in Culture Henrietta Lacks could scarcely have imagined her importance in future scientific research. When she died of cervical cancer in 1951, cells extracted from her tumour were the first human cells successfully grown in culture. Dubbed HeLa (pictured using fluorescence microscopy), they have since formed the basis for groundbreaking discoveries and are still extensively used worldwide. However, recent sequencing of their genome suggests caution is needed. Comparison with the reference human genome and healthy human cells reveals many abnormalities, including the presence of multiple copies of most chromosomes, changes in gene order, and higher expression of over 2000 genes. Some differences, such as rearrangements on chromosome 11, may have contributed to causing her cancer, but others could have arisen spontaneously while the cells were kept in culture. Although they remain useful tools, especially in cancer research, these anomalies highlight potential limitations of HeLa cells as a general model for human biology. Written by Emmanuelle Briolat — Research published in G3 Image provided courtesy of Science Photo Library Copyright Science Photo Library Any re-use of this image must be authorised by Science Photo Library
Pop-upView Separately
21 April 2013

Change in Culture

Henrietta Lacks could scarcely have imagined her importance in future scientific research. When she died of cervical cancer in 1951, cells extracted from her tumour were the first human cells successfully grown in culture. Dubbed HeLa (pictured using fluorescence microscopy), they have since formed the basis for groundbreaking discoveries and are still extensively used worldwide. However, recent sequencing of their genome suggests caution is needed. Comparison with the reference human genome and healthy human cells reveals many abnormalities, including the presence of multiple copies of most chromosomes, changes in gene order, and higher expression of over 2000 genes. Some differences, such as rearrangements on chromosome 11, may have contributed to causing her cancer, but others could have arisen spontaneously while the cells were kept in culture. Although they remain useful tools, especially in cancer research, these anomalies highlight potential limitations of HeLa cells as a general model for human biology.

Written by Emmanuelle Briolat

—

Infiltration Injection Humans may claim to have invented the hypodermic needle, but in fact, nature was plying them long before we came along. Through a vanishingly thin ‘needle’, certain viruses are able to infect bacteria, such as this Escherichia coli cell (large circle). The virus uses six fibres to rest on the bacterium, like a space shuttle on the moon, before piercing the surface with its tail (faded line emerging from small circle nearest bottom). Then, just as a doctor’s syringe delivers its payload, the virus uses this tube to inject the unfortunate E.coli cell with its own DNA – the genetic code of life. The cell then unwittingly creates thousands more virus copies from this blueprint, which eventually burst out, killing the bacterium. Understanding this process is important because viruses that attack bacteria in this way could offer a weapon against drug-resistant strains. Written by Jan Piotrowski — Ian Molineux Jun Liu University of Texas at Austin, USA Published in Science 339(6119): 576-579; Reprinted with permission from AAAS
Pop-upView Separately

Infiltration Injection

Humans may claim to have invented the hypodermic needle, but in fact, nature was plying them long before we came along. Through a vanishingly thin ‘needle’, certain viruses are able to infect bacteria, such as this Escherichia coli cell (large circle). The virus uses six fibres to rest on the bacterium, like a space shuttle on the moon, before piercing the surface with its tail (faded line emerging from small circle nearest bottom). Then, just as a doctor’s syringe delivers its payload, the virus uses this tube to inject the unfortunate E.coli cell with its own DNA – the genetic code of life. The cell then unwittingly creates thousands more virus copies from this blueprint, which eventually burst out, killing the bacterium. Understanding this process is important because viruses that attack bacteria in this way could offer a weapon against drug-resistant strains.

Written by Jan Piotrowski

—

Reading Genes

The Human Genome Project successfully decoded our genetic heritage. Since then science has discovered that most of this material lies unused within our cells. Epigenetics – how genes switch on and off – is paving the way for advances in regenerative medicine and stem cell research. Professor Wendy Bickmore here explains how two metres of the same genetic material gets packed into each body cell, inside a space narrower than a hundredth of a millimeter. It has to be highly folded. Many genes can’t then be reached by the machinery that ‘reads’ them and translates them into active proteins. So, folding affects which genes get switched on or off. When the wrong genes switch on or off cancer can result. Wendy’s research team looked at human chromosome 16. DNA in this region is folded differently in breast cancer cells than normal cells. Now they are trying to find out why.

Written by Brona McVittie

—

Funny Smells Even flies can be put off rotten food by its yucky smell. Scientists have discovered that fruit flies have special sensory cells to detect geosmin, a chemical produced by bacteria. This means they can avoid colonies of harmful microbes when feasting on yeast – their favourite food – on the surface of fermenting fruit. Flies don’t have noses but odour-sensing cells on their antennae and mouthparts (so they can’t join in the fund-raising stunts of today’s Red Nose Day in the UK). Fruit flies are used extensively for research into the role that genes play in the animal sense of smell, known as the olfactory system. Pictured is a fruit fly’s head with dots of colour marking different types of odour-sensing receptors, with superimposed letters denoting the gene sequences that keep them active. Written by Mick Warwicker — Rachel Jones Originally published under a Creative Commons Attribution license Published in PLoS Biology 6(5): e134
Pop-upView Separately

Funny Smells

Even flies can be put off rotten food by its yucky smell. Scientists have discovered that fruit flies have special sensory cells to detect geosmin, a chemical produced by bacteria. This means they can avoid colonies of harmful microbes when feasting on yeast – their favourite food – on the surface of fermenting fruit. Flies don’t have noses but odour-sensing cells on their antennae and mouthparts (so they can’t join in the fund-raising stunts of today’s Red Nose Day in the UK). Fruit flies are used extensively for research into the role that genes play in the animal sense of smell, known as the olfactory system. Pictured is a fruit fly’s head with dots of colour marking different types of odour-sensing receptors, with superimposed letters denoting the gene sequences that keep them active.

Written by Mick Warwicker

—

Source: bpod.mrc.ac.uk

Sticking Together Ever been defeated by a particularly tricky bit of flat-pack furniture? Even our cells struggle with DIY sometimes. Within a dividing cell, matching pairs of chromosomes must join up to exchange sections of DNA. This is a delicate process, and if the chromosomes fail to join or separate properly, new cells can end up with serious genetic abnormalities. Some complications are caused by structural faults in a molecular ‘velcro’ called cohesin, which holds the two chromosomes together. The chromosome pairs pictured come from dividing egg cells from mice lacking part of cohesin. In each case complete pairing has been disrupted: by a ‘fork’ (top left) ‘bubbles’ (top right and bottom left) or by failure to join altogether (bottom right). Knowing the crucial role of cohesin is a step towards understanding why some pregnancies fail in the early stages, as egg cells with chromosomal defects rarely survive for long after fertilisation. Written by Emma Stoye — Patricia Hunt Washington State University, USA Originally published under a Creative Commons Attribution license Published in PLoS Genetics 9(2): e1003241
Pop-upView Separately

Sticking Together

Ever been defeated by a particularly tricky bit of flat-pack furniture? Even our cells struggle with DIY sometimes. Within a dividing cell, matching pairs of chromosomes must join up to exchange sections of DNA. This is a delicate process, and if the chromosomes fail to join or separate properly, new cells can end up with serious genetic abnormalities. Some complications are caused by structural faults in a molecular ‘velcro’ called cohesin, which holds the two chromosomes together. The chromosome pairs pictured come from dividing egg cells from mice lacking part of cohesin. In each case complete pairing has been disrupted: by a ‘fork’ (top left) ‘bubbles’ (top right and bottom left) or by failure to join altogether (bottom right). Knowing the crucial role of cohesin is a step towards understanding why some pregnancies fail in the early stages, as egg cells with chromosomal defects rarely survive for long after fertilisation.

Written by Emma Stoye

—

Source: bpod.mrc.ac.uk