Biosphere

This is a good summary from Genetics Policy Center on how cloning is achieved and its uses.

View this amazing presentation with a nice cup of coffee and a cosy chair. Sit back and let life unfold before you.

Frans Lanting’s Lyrical View of Life

Scientists discover HMGA2. Gives one a good 1 cm more for homozygotes.

Scientists discover height gene

People who carry two copies of the “tall” version of the HMGA2 gene are up to 1cm taller than those who carry two copies of the “short” version.

The international team of researchers say the discovery could aid a greater understanding of the link between height and disease.

They predict in the journal Nature Genetics many other genes will now be uncovered that control height.

Although it has long been clear that genetics plays a key role in determining a person’s height, the genes involved have remained a mystery.

The latest study is a collaboration between Harvard University, the Children’s Hospital Boston, Oxford University and the Peninsula Medical School in Exeter.

They analysed the genomes of 5,000 white European patients, who gave DNA samples and details of their height and weight for medical studies into diabetes and heart disease.

They found just one tiny change in the HMGA2 gene had an impact on a person’s height.

The finding was confirmed by searching for the same two key versions of the gene in a further 30,000 patients.

Cancer link

Around 25% of white Europeans carry two copies of the “tall” version of the gene, while a similar proportion have two copies of the “short” version.

Carrying one copy of the “tall” version of the gene adds around 0.5cm to a person’s height, while two copies adds nearly a full centimetre.

Previous research has suggested that HMGA2 plays an important role in human growth.

Rare, severe mutations in the gene cause dramatic alterations of body size in mice and humans.

Researcher Dr Tim Frayling, of the Peninsula Medical School, said: “Height is a typical ‘polygenic’ trait, in other words many genes contribute towards making us taller or shorter.

“Clearly, our results do not explain why one person will be 6ft 5in (192 cms) and another only 4ft 10in (145cms).

“This is just the first of many that will be found, possibly as many as several hundred.”

A greater understanding of the genes behind height could also provide clues about risk of disease.

Taller people are statistically more likely to be at risk from prostate, bladder and lung cancer.

This suggests that the genes that regulate cell growth and division may also play a role in the uncontrolled cell proliferation characteristic of cancer.

Conversely, shorter people are known to have a higher risk of heart disease.

Professor Joel Hirschhorn, an expert in genetics at Harvard, said “This is the first convincing result that explains how DNA can affect normal variation in human height.

“Because height is a complex trait, involving a variety of genetic and non-genetic factors, it can teach us valuable lessons about the genetic framework of other complex traits, such as diabetes, cancer and other common human diseases.”

He added: “By defining the genes that normally affect stature, we might someday be able to better reassure parents that their child’s height is within the range predicted by their genes, rather than a consequence of disease.”

Five healthy babies have been born to provide stem cells for siblings with serious non-heritable conditions.

Read the article from New Scientist. Five “designer babies” created for stem cells

A summary of the research done on this famous allele. Includes basis for selection of this trait both in humans and other apes.

Wooding S. 2006 Phenylthiocarbamide: A 75-Year Adventure in Genetics and Natural Selection. Genetics.172(4): 2015–2023.

A good online tutorial on restriction enzymes and gel electrophoresis.

By Prentice Hall.

Molecular Biology Lab Bench Activity by ThereaKnapp Holtzclaw.

A free pdf book on genes and genetic conditions.
Provided by the US National Library of Medicine.

Good reference for the general.

Genetics Home Reference

Resource on conception control:

University of Michigan Health System - Birth Control Methods

Birth control methods

Baby Center - Restoring Fertility

From BBC News

UK scientists believe in the future they will be curing babies in the womb of serious diseases with the use of gene therapy.
The work is controversial not just because of the ethics but also safety concerns.

A few years ago France and the US suspended gene therapy trials after a child who had undergone treatment at the age of three developed cancer.

The British Society for Gene Therapy heard how trials were progressing.

Womb therapy

Gene therapy is a way of treating disease by either replacing damaged or abnormal genes with normal ones or by providing new genetic instructions to help fight disease.

These therapeutic genes can be transferred into the patient attached to a non-threatening virus or similar carrier “vector” which is injected it into the body.

Scientists have already successfully treated patients with haemophilia and infants with rare “bubbly boy” disease, who have no immune system, using gene therapy.

But gene therapy in children and adults has faced problems because the recipient’s body can mount an immune response and make antibodies that prevent the treatment working.

And there is also the risk that the treatment may trigger other diseases, like cancer.

The hope is that, at the foetal stage, the immune system is not yet developed sufficiently to prevent the effect of the implanted genes.

Scientists believe the treatment could also be more powerful in babies who are still developing and whose cells are rapidly multiplying.

Plus, it could provide a cure before the disease has had chance to cause any damage in the unborn child.

Dr Simon Waddington of University College London explained: “There are several advantages. For example, in cystic fibrosis, lung damage is actually occurring before birth.

“So, if you can get your gene therapy in before then, you might be able to stop the disease from happening.

“If you are going to treat adults it is often too late to reverse some of the damage.”

He stressed this was not meddling with gene traits to be passed on to future generations. “We are not modifying the children’s children, only treating that patient.”

He and colleagues at Imperial College have already successfully implanted corrective genes in foetal mice with disease.

And they have received a grant to test a gene therapy cure for the blood disorder haemophilia in unborn primates.

Dr Waddington said they still had another five years of testing in animals to do before they could think about move the technique into humans.

But he added: “The technologies are there to deliver and inject genes into babies if we find it is effective enough and safe enough.”

The scientists cannot yet exclude whether the genes might pass into the mother as well as the baby, for example.

Co-researcher Professor Charles Coutelle, at Imperial College, said: “The safety issue is something that will take time…and needs looking at very carefully.”

A Department of Health spokesperson said: “No human clinical trials of in utero gene therapy have ever taken place in the UK, nor is this considered to be feasible in the next few years.”

An interesting article on Sexual Reproduction by Liza Gross, PLOS Biology.
PLOS Biology - Liza Gross Gross L (2007) Who Needs Sex (or Males)

If you own a birdbath, chances are you’re hosting one of evolutionary biology’s most puzzling enigmas: bdelloid rotifers. These microscopic invertebrates—widely distributed in mosses, creeks, ponds, and other freshwater repositories—abandoned sex perhaps 100 million years ago, yet have apparently diverged into nearly 400 species. Bdelloids (the “b” is silent) reproduce through parthenogenesis, which generates offspring with essentially the same genome as their mother from unfertilized eggs. Biologists have yet to find males, hermaphrodites, or any trace of meiosis—the process that creates sex cells—challenging the long-held assumption that evolutionary success requires genetic exchange.

The genetic variation created by meiosis and fertilization, theory holds, bolsters a species’s capacity to weather shifting environmental conditions or resist rapidly evolving parasites. (During meiosis, the genome splits in two, and chromosome pairs swap bits of their DNA; during fertilization, the sex cells fuse to restore the complete genome.) Many multicellular eukaryotes pass through a sexual and asexual phase in their life cycle. But eschewing sex altogether, à la bdelloids, is not theoretically consistent with a long-lived evolutionary life span or extensive species diversification.

In a new study, Diego Fontaneto, Timothy Barraclough, and colleagues developed new statistical techniques for combined molecular and morphological analyses of rotifers to test the notion that species diversification requires sex. The researchers show that, despite an ancient aversion for interbreeding, bdelloids display evolutionary patterns similar to those seen in sexually reproducing taxa. How they have avoided the pitfalls of a lifestyle widely regarded as evolutionary suicide remains an open question.

Bdelloids have remained such an enduring enigma in part because biologists are still debating whether species exist as true evolutionary entities. And if they do, what forces determine how they diverge? Traditional taxonomy relies on morphological differences to classify species, but it can’t distinguish whether such differences reflect physical variations among a group of clones or adaptations among independently evolving populations. In the traditional view of species diversification, interbreeding promotes cohesion within a population—maintaining the species—and barriers to interbreeding (called reproduction isolation) promote species divergence. With no interbreeding to maintain cohesion, the thinking goes, asexual taxa might not diversify into distinct species.

Scanning electron micrographs showing morphological variation of bdelloid rotifers and their jaws. Have these asexual animals really diversified into evolutionary species? (Image: Diego Fontaneto)

Fontaneto et al. defined species as independently evolving, distinct populations (or units of diversity) subject to distinct evolutionary mechanisms. They predicted that if factors other than interbreeding—such as niche specialization—controlled species cohesion and divergence, then asexual taxa should diverge along the same lines as sexually reproducing organisms. And if this were the case, they would expect to find genetic and morphological cohesion within independently evolving populations and divergence between them.

To detect independently evolving populations, the researchers analyzed marker genes isolated from clones of bdelloids collected from diverse habitats around the world. They constructed evolutionary trees using both mitochondrial and nuclear DNA sequences (the molecular “barcode” cox1and 28S ribosomal DNA sequences, respectively) to identify species within the samples. For the morphological analysis, they measured the size and shape of the rotifers’ jaws (called trophi).

The morphological results largely fell in line with traditional taxonomic classifications for most bdelloid species. And species identified as related on the DNA trees typically had similar morphology. The correspondence between the molecular and morphological results suggests that the majority of traditionally identified bdelloid species are what’s known as monophyletic—individuals in the same species assort together on the evolutionary tree and share a common ancestor. Only two of these traditional, monophyletic species showed significant variation in trophi size or shape among the populations; both also showed significant divergence in the DNA trees.

Using statistical models to determine the likely origin of the observed DNA tree branching patterns, the researchers show that these distinct monophyletic genetic clusters represent independently evolving entities (rather than variations within a single asexual population). But what caused them to evolve independently? Are they geographically isolated populations that evolved under neutral selection, or did they evolve into ecologically discrete species as a result of divergent selection pressures on trophi morphology?

If bdelloids have experienced divergent selection, the researchers explain, they would expect to see high variation in trophi traits between species, and low intraspecies variation (compared to neutral changes). And that’s what they found—bdelloids have experienced divergent selection on trophi size (and to a lesser degree, on trophi shape) at the species level.

Altogether, these results show that the asexual bdelloids have indeed experienced divergent selection on feeding morphology, most likely as they adapted to different food sources found in different niches. By showing that asexual organisms have diverged into “independently evolving and distinct entities,” the researchers argue, this study “refutes the idea that sex is necessary for diversification into evolutionary species.” They hope others use their approach to study mechanisms underlying species divergence in sexual taxa to clarify the hazy nature of species and biological diversity.