Dolly's aging heirs offer good news about cloned animals
Dolly herself died young after developing osteoarthritis, infection; but her clones are healthy

The heirs of Dolly the sheep are enjoying a healthy old age, proving cloned animals can live normal lives and offering reassurance to scientists hoping to use cloned cells in medicine.

Dolly, cloning’s poster child, was born in Scotland in 1996. She died prematurely in 2003, aged six, after developing osteoarthritis and a lung infection, raising concerns that cloned animals may age more quickly than normal offspring.

Now researchers have allayed those fears by reporting that 13 cloned sheep, including four genomic copies of Dolly, are still in good shape at between seven and nine years of age, or the equivalent of 60 to 70 in human years.

“Overall, the results are suggesting that these animals are remarkably healthy,” said Kevin Sinclair of the University of
Nottingham, whose team reported their findings in the journal Nature Communications on Tuesday.

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Changes in Teen Brain Structure Provide Clues to Onset of Mental Health Problems

Scientists have mapped the structural changes that occur in teenagers’ brains as they develop, showing how these changes may help explain why the first signs of mental health problems often arise during late adolescence.

In a study published today in the Proceedings of the National Academy of Sciences, researchers from the University of Cambridge and University College London (UCL) used magnetic resonance imaging (MRI) to study the brain structure of almost 300 individuals aged 14-24 years old.

By comparing the brain structure of teenagers of different ages, they found that during this important period of development, the outer regions of the brain, known as the cortex, shrink in size, becoming thinner. However, as this happens, levels of myelin – the sheath that ‘insulates’ nerve fibres, allowing them to communicate efficiently – increase within the cortex.

“Adolescence is associated with genomically patterned consolidation of the hubs of the human brain connectome” by Kirstie J. Whitaker, Petra E. Vértes, Rafael Romero-Garcia, František Váša, Michael Moutoussis, Gita Prabhu, Nikolaus Weiskopf, Martina F. Callaghan, Konrad Wagstyl, Timothy Rittman, Roger Tait, Cinly Ooi, John Suckling, Becky Inkster, Peter Fonagy, Raymond J. Dolan, Peter B. Jones, Ian M. Goodyer, the NSPN Consortium, and Edward T. Bullmore in PNAS. Published online July 25 2016 doi:10.1073/pnas.1601745113

Previously, myelin was thought mainly to reside in the so-called ‘white matter’, the brain tissue that connects areas of the brain and allows for information to be communicated between brain regions. However, in this new study, the researchers show that it can also be found within the cortex, the ‘grey matter’ of the brain, and that levels increase during teenage years. In particular, the myelin increase occurs in the ‘association cortical areas’, regions of the brain that act as hubs, the major connection points between different regions of the brain network. image is for illustrative purposes only.
Jim Carter and Joanne Froggatt ALS Ice Bucket Challenge
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Ice Bucket Challenge leads to ALS breakthrough!!!!!!

The ALS Association raised more than $100m (£76m) and contributed $1m to Project MinE - an international study to sequence the genomes of at least 15,000 people with ALS.

It has led to the discovery of a new ALS gene, NEK1, which now ranks among the most common genes that contribute to the disease.

Read more here!

Cloning does not cause long-term health issues, study finds

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wenty years ago Dolly – the first mammal to be cloned – was born to global fanfare. The ground-breaking animal has long been deceased but genomic copies are living on healthily.

Four sheep, all female Finn-Dorset clones, derived from the same mammary gland cell line Dolly was created from have all aged with no major issues and show no more than mild signs of the degenerative osteoarthritis suffered by the original clone.

Debbie, Denise, Dianna and Daisy, all nine, were born in 2007 and have outlived Dolly, who died aged 6.5 years old. Their good health is being hailed as a success for cloning as there’s “no evidence” of a “detrimental long-term” health effect in the miniature flock. The results will help to quell fears that clones typically age faster than animals which are born naturally.

The foursome make up part of 13 sheep cloned and medically examined by an international team of biologists, which has published its findings in the journal Nature Communications.

“There’s a cohort of embryos that implant, go to term, produce viable offspring, which then over the next eight to 10 years age normally and they’re healthy,” Kevin Sinclair, the lead author of the work, from Nottingham University, told WIRED.

“We can say with confidence that at least some embryos are able to successfully complete this whole process.”

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It looks like some sort of press conference is being held, but the important thing to note here is that the three women attending Mason appear, for all intents and purposes, to be the same ones that did the underwater salvage. I like how each of them has an identical dress but a different shoulder insignia. Is that supposed to be some sort of rank? We know these women aren’t human, but that’s likely a fact not made public. Is this arbitrary assigning of hierarchy–something unimportant to Boomers–another effort to hide things from the public?

JUST THE FAQS: How Cells Make Many Proteins from a Single Gene

“One big surprise that came out of Human Genome Project was the discovery that humans have fewer genes than expected — far fewer than you’d expect, compared to simpler organisms,” Joseph A­­dams, PhD, professor of pharmacology in UC San Diego School of Medicine. “We now know that’s because our cells can produce many different proteins based on the same recipe encoded in a single gene — a mechanism known as splicing.”

Adams and his lab study splicing and the enzymes that help control it. Here, JUST THE FAQS breaks down their latest study, published in Molecular Cell.

What is splicing?

The central dogma of life is this process: genes (DNA) in the cell’s nucleus are transcribed into messenger RNA (mRNA), which then moves out of the nucleus and into the cytoplasm, where cellular machinery translates that recipe to assemble proteins. Proteins make up the bulk of the cell and do most of the work essential to life.

Splicing is a cell’s way of editing genes before they get translated into proteins. To do this, enzymes in the nucleus splice pre-mRNA, removing parts of the code that don’t encode proteins and joining together the sections that do. The final product is mature mRNA, which is what moves on to the cytoplasm. There’s some wiggle room in what’s spliced out or left in — hence the complexity of human biology, despite our surprisingly few genes in the genome.

Cells must tightly regulate splicing to ensure that only the right proteins are being made at the right time. Enzymes and other proteins help do this. For example, SR factors are proteins that initiate mRNA splicing in the nucleus. Kinases are enzymes that keep tabs on the SR factors.

What are kinases and how are they involved in mRNA splicing?

Kinases are enzymes in a cell that tag proteins with phosphate chemical groups — a process known as phosphorylation. This seemingly simple act can dramatically alter a protein’s function, location in the cell, or very existence.

Kinases can also influence mRNA splicing. The CLK family of kinases, for example, are located in the nucleus, where they phosphorylate SR factors and mobilize them from storage. Yet CLKs don’t release the SR factors, effectively inactivating them.

“For many years it was accepted that CLKs are critical for mobilizing SR proteins,” Adams said. “The problem is that, paradoxically, too much CLK inhibits splicing. For us, that was a dilemma. After all, how can CLKs both activate and inhibit splicing?”

What did the researchers find in this study?

In this latest study, Adams and team made an unexpected discovery: CLKs in the nucleus don’t let go of SR factors until another kinase, SRPK, comes along. 

Previously, SRPK kinases were thought to be confined to the cytoplasm. Now Adams’ team has found SRPKs actually move into the nucleus when stimulated with growth factors. In the nucleus, SRPKs are captured by resident CLK kinases and the two enzymes form complexes. That complex releases SR factors from CLK. Once SR factors are released, they can couple with and activate the spliceosome — the cellular machinery that binds and splices pre-mRNA.

This finding explains why elevated CLK levels inhibit splicing — more CLK means more sequestered SR factors and more SRPK needed to free them.

Why is this important?

According to Adams, it’s unprecedented to find two kinases that join up and function together. What’s more, he said, “splicing errors occur in many human diseases. CLK and SR levels in particular are elevated in breast and other cancers. Knowing how to regulate this system is critical to understanding the causes of these diseases and finding weaknesses we could exploit with new therapeutics.”

What’s next?

Moving forward, Adams and his team want to better understand the nature of the SRPK-CLK complex, how it regulates splicing on a global level and how many genes are affected. In addition, they hope to discover elements other than growth factors that balance the movement of SRPK in and out of the nucleus.

Image caption: SRPK1 (green) migrating to the nucleus (blue) in response to CLK1