19 June 2013 Cutting the Brakes Any organism more complex than a single-celled amoeba faces a challenge – how to grow from a single cell to a more complicated creation in an organised way. These neat ovals are fruit fly embryos, stained to show the activity patterns of a range of different genes that are important in early development. These tightly-controlled stripes set out the body plan for the developing fly, defining head from tail and laying out the different sections of the animal. But things can go wrong. The top row are normal fly embryos, while the bottom row all carry a fault in a gene called brakeless (also known by the evocative names “scribbler” and “master of thick veins”). The patterns of gene activity are subtly shifted and embryos lacking brakeless grow up to be stubby and deformed, revealing how the complex interplay between different genes helps to lay down the instructions for building life. Written by Kat Arney — Mattias Mannervik Stockholm University, Sweden Originally published under a Creative Commons Attribution license Published in PLoS Biol 5(6): e145
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19 June 2013

Cutting the Brakes

Any organism more complex than a single-celled amoeba faces a challenge – how to grow from a single cell to a more complicated creation in an organised way. These neat ovals are fruit fly embryos, stained to show the activity patterns of a range of different genes that are important in early development. These tightly-controlled stripes set out the body plan for the developing fly, defining head from tail and laying out the different sections of the animal. But things can go wrong. The top row are normal fly embryos, while the bottom row all carry a fault in a gene called brakeless (also known by the evocative names “scribbler” and “master of thick veins”). The patterns of gene activity are subtly shifted and embryos lacking brakeless grow up to be stubby and deformed, revealing how the complex interplay between different genes helps to lay down the instructions for building life.

Written by Kat Arney

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Source: bpod.mrc.ac.uk

18 June 2013 On the Fringe As any style icon knows, a neat fringe is essential for a chic hairdo. Similarly, the fruit fly’s fringe gene is vital for looking sharp. It’s responsible for forming the edges of a fly’s wings, and is switched on in a tightly-controlled area in the developing wing as a tiny maggot transforms into an adult fly. Pictured is a neat stripe of cells that have switched on fringe, coloured in green, marking where the edge of the wing should go. Humans have three versions of FRINGE, called LUNATIC FRINGE, MANIC FRINGE and RADICAL FRINGE, which help to shape our limbs and other body parts. Inherited faults in LUNATIC FRINGE cause severe problems with the development of the spine, and although the gene’s name may seem funny, it’s not amusing for families affected by the disease, so it’s usually referred to just as LFNG. Written by Kat Arney — Thomas Klein Heinrich-Heine-University Düsseldorf, Germany Originally published under a Creative Commons Attribution license Published in PLoS ONE 7(11): e49007
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18 June 2013

On the Fringe

As any style icon knows, a neat fringe is essential for a chic hairdo. Similarly, the fruit fly’s fringe gene is vital for looking sharp. It’s responsible for forming the edges of a fly’s wings, and is switched on in a tightly-controlled area in the developing wing as a tiny maggot transforms into an adult fly. Pictured is a neat stripe of cells that have switched on fringe, coloured in green, marking where the edge of the wing should go. Humans have three versions of FRINGE, called LUNATIC FRINGE, MANIC FRINGE and RADICAL FRINGE, which help to shape our limbs and other body parts. Inherited faults in LUNATIC FRINGE cause severe problems with the development of the spine, and although the gene’s name may seem funny, it’s not amusing for families affected by the disease, so it’s usually referred to just as LFNG.

Written by Kat Arney

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Source: bpod.mrc.ac.uk

17 June 2013 Swapping Legs You might have seen tiny fruit flies buzzing around your bananas on a summer day, but have you ever stopped to look more closely? Scientists have studied these little insects for more than a century, and they have revealed many important genes involved in human growth, health and disease. You’re unlikely to have spotted a fly like this in your fruit bowl though – it has an extra pair of legs where its antennae should be, as a result of a mutation in a gene called antennapedia (literally translated as “antenna feet”). There are several similar genes in humans known as HOX genes, that are responsible for organising parts of our body plan as we grow in the womb. Unusual fruit fly mutations like this have helped researchers to unravel the complex processes that shape our bodies, and discover common patterns and pathways across the whole animal kingdom. Written by Kat Arney — Originally published under a Creative Commons Attribution license (CC-BY-SA 3.0, Toony)
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17 June 2013

Swapping Legs

You might have seen tiny fruit flies buzzing around your bananas on a summer day, but have you ever stopped to look more closely? Scientists have studied these little insects for more than a century, and they have revealed many important genes involved in human growth, health and disease. You’re unlikely to have spotted a fly like this in your fruit bowl though – it has an extra pair of legs where its antennae should be, as a result of a mutation in a gene called antennapedia (literally translated as “antenna feet”). There are several similar genes in humans known as HOX genes, that are responsible for organising parts of our body plan as we grow in the womb. Unusual fruit fly mutations like this have helped researchers to unravel the complex processes that shape our bodies, and discover common patterns and pathways across the whole animal kingdom.

Written by Kat Arney

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Originally published under a Creative Commons Attribution license (CC-BY-SA 3.0, Toony)

Source: bpod.mrc.ac.uk

16 June 2013 Baby Brown Fat Not all fat is white and wobbly. Some appears brown, because it’s full of tiny cellular factories called mitochondria, which generate heat and chemical energy. This brown fat is leaner and healthier than white fat, as it uses up fat molecules as well as storing them. Small rodents have it in abundance and use it to produce heat when they wake up from hibernation. Only tiny amounts of brown fat exist in adult humans, but newborn babies have a patch around and between their shoulders, as shown on this reconstruction (brown fat coloured green). MRI scans, biopsies and biomedical tests have been used to map its position. Brown fat helps keep babies warm, but most of it disappears as they grow up. Scientists don’t yet know why or how this happens. A better understanding could uncover new ways to fight obesity. Written by Emma Stoye — Sven Enerbäck University of Gothenburg, Sweden Reprinted by permission from Macmillan Publishers Ltd: Nature Medicine Copyright 2013 Published in Nature Medicine 19: 631-634
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16 June 2013

Baby Brown Fat

Not all fat is white and wobbly. Some appears brown, because it’s full of tiny cellular factories called mitochondria, which generate heat and chemical energy. This brown fat is leaner and healthier than white fat, as it uses up fat molecules as well as storing them. Small rodents have it in abundance and use it to produce heat when they wake up from hibernation. Only tiny amounts of brown fat exist in adult humans, but newborn babies have a patch around and between their shoulders, as shown on this reconstruction (brown fat coloured green). MRI scans, biopsies and biomedical tests have been used to map its position. Brown fat helps keep babies warm, but most of it disappears as they grow up. Scientists don’t yet know why or how this happens. A better understanding could uncover new ways to fight obesity.

Written by Emma Stoye

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Source: bpod.mrc.ac.uk

15 June 2013 Stressed for Success There’s a lot to learn from watching how life adapts. Myofibroblasts are stretchy cells that help to repair our organs – contracting to bring the edges of a wound together and then self-destructing like tiny dissolvable stiches. These rat myofibroblasts have been grown on differently-sized artificial ‘islands’, putting strain on their criss-crossing stress fibres (highlighted here with multi-coloured fluorescent dyes). Forced to stretch out, the cells adapt and remodel – the cell on the large island (right) has developed more stress fibres than the ‘relaxed’ cell on the smaller island (left, 200 million times smaller than The Isle of Man). Watching how myofibroblasts respond to stress tells us a great deal about how they cope inside our bodies, and what happens when they’re pushed too far – malfunctioning myofibroblasts left behind after a wound has healed can build up into scar tissue, sometimes leading to severe conditions like pulmonary fibrosis. Written by John Ankers — Boris Hinz University of Toronto, Canada Originally published under a Creative Commons Attribution license Published in PLoS ONE 8(5): e64560
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15 June 2013

Stressed for Success

There’s a lot to learn from watching how life adapts. Myofibroblasts are stretchy cells that help to repair our organs – contracting to bring the edges of a wound together and then self-destructing like tiny dissolvable stiches. These rat myofibroblasts have been grown on differently-sized artificial ‘islands’, putting strain on their criss-crossing stress fibres (highlighted here with multi-coloured fluorescent dyes). Forced to stretch out, the cells adapt and remodel – the cell on the large island (right) has developed more stress fibres than the ‘relaxed’ cell on the smaller island (left, 200 million times smaller than The Isle of Man). Watching how myofibroblasts respond to stress tells us a great deal about how they cope inside our bodies, and what happens when they’re pushed too far – malfunctioning myofibroblasts left behind after a wound has healed can build up into scar tissue, sometimes leading to severe conditions like pulmonary fibrosis.

Written by John Ankers

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Source: bpod.mrc.ac.uk

14 June 2013 Insulation Inspiration Neurons are like electric cables. To carry currents effectively, they must have a covering of insulation around their long projections. When this fatty layer – called the myelin sheath – breaks down, the effect on the nervous system can be disastrous. Currently there’s no cure for this deterioration, leaving sufferers of myelin-wasting problems, like Pelizaeus-Merzbacher disease, no hope of recovery. However, transplanting undeveloped cells, whose mature form (shown in red) can repair the insulation, could be a promising therapy … if a plentiful supply of these precursors can be found. To solve this, scientists used viruses to alter the genetic make-up of a common cell type in mice. This causes them to shape-shift into precursor cells, which when injected into mouse brain, leads to myelin growth. Proof that reprogrammed and naturally-occurring precursors behave similarly, gives hope that the technique could one day provide the raw materials for a Pelizaeus-Merzbacher disease therapy. Written by Jan Piotrowski — Marius Wernig Stanford University School of Medicine, USA Reprinted by permission from Macmillan Publishers Ltd: Nature Biotechnology Copyright 2013 Published in Nature Biotechnology 31, 434-439
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14 June 2013

Insulation Inspiration

Neurons are like electric cables. To carry currents effectively, they must have a covering of insulation around their long projections. When this fatty layer – called the myelin sheath – breaks down, the effect on the nervous system can be disastrous. Currently there’s no cure for this deterioration, leaving sufferers of myelin-wasting problems, like Pelizaeus-Merzbacher disease, no hope of recovery. However, transplanting undeveloped cells, whose mature form (shown in red) can repair the insulation, could be a promising therapy … if a plentiful supply of these precursors can be found. To solve this, scientists used viruses to alter the genetic make-up of a common cell type in mice. This causes them to shape-shift into precursor cells, which when injected into mouse brain, leads to myelin growth. Proof that reprogrammed and naturally-occurring precursors behave similarly, gives hope that the technique could one day provide the raw materials for a Pelizaeus-Merzbacher disease therapy.

Written by Jan Piotrowski

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Source: bpod.mrc.ac.uk

13 June 2013 Cancer Maps These charts show the mutated DNA of two children with acute lymphoblastic leukaemia. The coloured bands illustrate where large areas of the children’s DNA, called chromosomes (1–22, X and Y), once broke apart and stuck back together in an unnatural arrangement (chromosome 5 joined to chromosome 18, for example), triggering their disease. There are vital clues here as to when this event happened: the children are twins, and their identically jumbled DNA suggests that the cancer originated before birth, in the womb. Other DNA mutations (shown with purple, blue or red dashes around the circumference of the rings) are unique to each twin, showing how their conditions diverged and developed separately after they were born. Unravelling the early time-lines of childhood cancers is vital for pre-natal diagnosis and post-natal treatment, especially as the disease can develop to be just as individual as we are. Written by John Ankers — Mel Greaves Richard Houlston Institute of Cancer Research, UK Published in PNAS 110(18): 7429-7433
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13 June 2013

Cancer Maps

These charts show the mutated DNA of two children with acute lymphoblastic leukaemia. The coloured bands illustrate where large areas of the children’s DNA, called chromosomes (1–22, X and Y), once broke apart and stuck back together in an unnatural arrangement (chromosome 5 joined to chromosome 18, for example), triggering their disease. There are vital clues here as to when this event happened: the children are twins, and their identically jumbled DNA suggests that the cancer originated before birth, in the womb. Other DNA mutations (shown with purple, blue or red dashes around the circumference of the rings) are unique to each twin, showing how their conditions diverged and developed separately after they were born. Unravelling the early time-lines of childhood cancers is vital for pre-natal diagnosis and post-natal treatment, especially as the disease can develop to be just as individual as we are.

Written by John Ankers

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Source: bpod.mrc.ac.uk

12 June 2013 Hairy Humans Our ancient hominin relatives who wandered around Africa were a lot hairier than most of us modern humans. However a few rare examples of people who grow excessive amounts of hair are still found today. Pictured are males, and a female (bottom right with magnified inset), of a particularly hirsute Mexican family. It is thought that such people are exhibiting genetic atavism – whereby genes that were once responsible for an ancestral trait, such as a full coat of body hair, and that have altered their expression over the course of human evolution, have somehow reverted to their ancestral pattern. In the case of this Mexican family, researchers have found a chromosomal rearrangement that affects a gene called FGF13. The FGF13 protein is expressed in hair follicles and is thought to regulate their growth and activity, possibly explaining why this gene’s misregulation has caused an ancestral-like overgrowth of hair. Written by Ruth Williams — Angela Christiano Columbia University, USA Published in PNAS 110(19) 7790-7795
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12 June 2013

Hairy Humans

Our ancient hominin relatives who wandered around Africa were a lot hairier than most of us modern humans. However a few rare examples of people who grow excessive amounts of hair are still found today. Pictured are males, and a female (bottom right with magnified inset), of a particularly hirsute Mexican family. It is thought that such people are exhibiting genetic atavism – whereby genes that were once responsible for an ancestral trait, such as a full coat of body hair, and that have altered their expression over the course of human evolution, have somehow reverted to their ancestral pattern. In the case of this Mexican family, researchers have found a chromosomal rearrangement that affects a gene called FGF13. The FGF13 protein is expressed in hair follicles and is thought to regulate their growth and activity, possibly explaining why this gene’s misregulation has caused an ancestral-like overgrowth of hair.

Written by Ruth Williams

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Source: bpod.mrc.ac.uk

11 June 2013 Making Moulds These coloured tiles may look like designs for fabrics or furnishings but, rather than being made of cloth, they’re crafted from living cells. Scientists have created miniature moulds that can organise and support several different types of cells at the same time – in these examples one type of cell is stained green, while the other is red. As well as looking beautiful, the technology has a vital purpose that could save thousands of lives in the future. Donor organs for transplantation are in short supply around the world, and there are problems with rejection if the match isn’t perfect. But organs are a complex arrangement of many different types of cells, and are currently tricky to grow in the lab. Making ‘moulded’ organs using this technique could solve the problem, and the researchers have already shown that they can create functioning liver tissue that can be transplanted into mice. Written by Kat Arney — Sangeeta Bhatia Massachusetts Institute of Technology, USA Reprinted by permission from Macmillan Publishers Ltd: Nature Communications Copyright 2013 Published in Nature Communications 4:1847
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11 June 2013

Making Moulds

These coloured tiles may look like designs for fabrics or furnishings but, rather than being made of cloth, they’re crafted from living cells. Scientists have created miniature moulds that can organise and support several different types of cells at the same time – in these examples one type of cell is stained green, while the other is red. As well as looking beautiful, the technology has a vital purpose that could save thousands of lives in the future. Donor organs for transplantation are in short supply around the world, and there are problems with rejection if the match isn’t perfect. But organs are a complex arrangement of many different types of cells, and are currently tricky to grow in the lab. Making ‘moulded’ organs using this technique could solve the problem, and the researchers have already shown that they can create functioning liver tissue that can be transplanted into mice.

Written by Kat Arney

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Source: bpod.mrc.ac.uk

10 June 2013 Fatal Attraction It’s a biological booby trap. Female A. stephensi mosquitos are standing over H. subflexa caterpillars (alive on the left, and dead on the right). But it’s not the caterpillar itself that’s so attractive to the mosquitos, rather what’s inside them – a deadly, yet irresistible, fungus. A minute’s contact with the fungal carriers is all it takes to infect and kill the mosquitos. In the future, the fatal fungus (B. Bassiana, seen as the white ‘fur’ sporulating out from the caterpillar cadavers on the right) may be used as a biopesticide, coated onto the surfaces of walls and nests, diverting mosquitos away from homes or schools, and infecting malaria carriers like A. stephensi before they can transmit their own deadly disease. Written by John Ankers — Thomas Baker Pennsylvania State University, USA Originally published under a Creative Commons Attribution license Published in PLoS ONE 8(5): e62632
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10 June 2013

Fatal Attraction

It’s a biological booby trap. Female A. stephensi mosquitos are standing over H. subflexa caterpillars (alive on the left, and dead on the right). But it’s not the caterpillar itself that’s so attractive to the mosquitos, rather what’s inside them – a deadly, yet irresistible, fungus. A minute’s contact with the fungal carriers is all it takes to infect and kill the mosquitos. In the future, the fatal fungus (B. Bassiana, seen as the white ‘fur’ sporulating out from the caterpillar cadavers on the right) may be used as a biopesticide, coated onto the surfaces of walls and nests, diverting mosquitos away from homes or schools, and infecting malaria carriers like A. stephensi before they can transmit their own deadly disease.

Written by John Ankers

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Source: bpod.mrc.ac.uk