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Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts | News Archive June 24, 2013

 
Transposons are characterised as ‘jumping’ because they can change their position within the
genome, thereby creating or reversing mutations. This process, known as DNA transposition,
plays a critical role in creating genetic diversity and enabling species to adapt and evolve.









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Why our prehistoric 'jumping' genes don't send us into meltdown

A team of researchers, led by academics at The University of Nottingham, UK, has explained why the so-called ‘jumping genes’ found in most living organisms don’t ultimately kill off their hosts, putting an end to a long-standing scientific mystery.

The study reveals for the first time how the movement and duplication of segments of DNA known as transposons, is regulated. This prevents a genomic meltdown, and instead enables transposons to live in harmony with their hosts — including humans.

Transposons were discovered in the 1940s by Barbara McClintock, who was rewarded in 1983 with the Nobel Prize for Physiology or Medicine. Ancient relics of these ‘jumping genes’, as they are sometimes called, make up 50 per cent of the DNA in humans.

They are characterised as ‘jumping’ because they can change their position within the genome, thereby creating or reversing mutations. This process, known as DNA transposition, plays a critical role in creating genetic diversity and enabling species to adapt and evolve.

Junk DNA


Transposons don’t just jump from one location to another; they usually leave behind a copy of themselves at their original location. Left unchecked, this would lead to an exponential increase in their numbers. Exponential growth is always unsustainable, and in the case of transposons they would quickly kill their host.


Because this doesn’t happen, clearly some form of regulation is taking place within the genome. For a long time, scientists have understood that an enzyme called transposase, which is critical to the whole transposition process, also apparently brings it under control.

How this actually occurs has, however, remained a mystery — until now. For the first time, the new study, carried out by researchers at The University of Nottingham, The University of Cambridge and the Fred Hutchinson Cancer Centre in Seattle, successfully identified the mechanism through which DNA transposition is regulated.

Ingenious mechanism

Ronald Chalmers, Professor of Molecular and Cellular Biology at The University of Nottingham, said “A successful parasite is not fatal to its host but lives in harmony with it. It was while doing some biochemistry research that we stumbled upon the solution. It was so simple that initially it was hard to appreciate the brilliance of it. It was a real forehead-slapping moment and seems a wonder that it was not discovered years ago.”

“In theory, transposons should just keep on increasing and kill us,” said Dr Karen Lipkow, from the Department of Biochemistry, University of Cambridge, and the Babraham Institute. “What we have identified is an ingenious mechanism which prevents this from happening by conferring autoregulation. The process is very simple, but it explains so much.”

A biochemical analysis of a mariner-family transposon from the human genome gave the first indication of the mechanism. The team then expanded this concept using a computer model, which allowed them to simulate events on an evolutionary timescale, before carrying out further biochemical experiments.

Genomic parasites

Transposase is important to the genetic ‘jump’ of transposons because it catalyses the whole process. It does this by binding to specific sites at either end of the transposon, and then bringing these together to create a nucleoprotein complex that effectively performs a molecular ‘cut and paste, moving the transposon DNA to a new location.


The study found that once a certain number of copies of the transposon have been created, the transposase concentration rises above a critical threshold and begins to saturate its own binding sites.

As clusters of the enzyme compete for binding sites, they interfere with each other and the transposition process is halted.


Using the computer model, the researchers were able to show that doubling the transposon copy number halves the rate of transposition. This is a crucial insight as it reveals an underlying self-righting mechanism for homeostasis. In a nutshell, it makes the transposon’s genetic burden on the host constant and predictable, and brings an uneasy harmony to the relationship.

The paper appears in eLife, a prestigious new journal published jointly by The Wellcome Trust, The Howard Hughes Medical Institute and The Max Planck Institute. It can be found at: http://elife.elifesciences.org/content/2/e00668

The University of Nottinghamhas 42,000 students at award-winning campuses in the United Kingdom, China and Malaysia. It was ‘one of the first to embrace a truly international approach to higher education’, according to the Sunday Times University Guide 2013. It is also one of the most popular universities among graduate employers, one of the world’s greenest universities, and winner of the Times Higher Education Award for ‘Outstanding Contribution to Sustainable Development’. It is ranked in the UK's Top 10 and the World's Top 75 universities by the Shanghai Jiao Tong and the QS World Rankings.

More than 90 per cent of research at The University of Nottingham is of international quality, according to the most recent Research Assessment Exercise. The University aims to be recognised around the world for its signature contributions, especially in global food security, energy & sustainability, and health. The University won a Queen’s Anniversary Prize for Higher and Further Education for its research into global food security.

Original press release:http://www.nottingham.ac.uk/news/pressreleases/2013/june/why-our-prehistoric,-parasitic-jumping-genes-dont-send-us-into-meltdown.aspx