Platypus missing link in the Early History of Mammals

Researches have unraveled the genetic make up of one of the world’s strangest mammals. Teams of researches located in the UK have analysed the DNA blueprint of Australia’s very own Platypus. The platypus is thought to have diverged from a common ancestor shared with humans approximately 170 million years ago.

The species has many features that are unique to mammals; for example it has fur and rears its young on milk. However, it also shows reptile-like characteristics; the females lay eggs and the males produce venom. Some features, such as a specialized system in the platypus bill that uses electricity to detect food under water (electro-reception), are unique to monotremes. The researchers found that these diverse characteristics are mirrored by a patchwork of genes resembling those from reptiles, birds and other mammals.
Lead researcher Chris Ponting from the MRC Functional Genomics Unit at the University of Oxford said "The platypus genome is extremely important because it is the missing link in our understanding of how we and other mammals first evolved. This is our ticket back in time to when all mammals laid eggs while suckling their young on milk. It also provides an essential background to future advances in understanding mammalian biology and evolution."

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Further Reading
http://www.embl.org/aboutus/news/press/2008/07may08/index.html

Humans Faced Extinction in Middle Palaeolithic Era

An extensive study into genetics has revealed that humans could have potentially become extinct some 70, 000 years ago. Scientific analysis has made apparent that the numbers of our predecessors on a global basis may have at one point in the Middle Palaeolithic era (between 200, 000- 35, 000 years ago) plummeted to a mere 2000 individuals, prior to growing again in the beginning of the Stone Age. This finding came about through the Genographic Project, an investigation that was launched in 2005 with the aim of using genetics to gain a broader understanding of anthropology.

The project’s director Spencer Wells of the National Geographic Society remarked,

”This study illustrates the extraordinary power of genetics to reveal insights into some of the key events in our species' history. Tiny bands of early humans, forced apart by harsh environmental conditions, coming back from the brink to reunite and populate the world. Truly an epic drama, written in our DNA."

The study incorporated findings from previous investigations which, through the analysis of mitochondrial DNA that is passed onto offspring through their mothers, concluded that a maternal ancestor to all modern human beings lived in Africa about 200, 000 years ago. This new study examined the mitochondrial DNA of the Khoi and San people in South Africa who are believed to have diverged evolutionarily from other people between 90,000 and 150,000 years ago. It was concluded from this study that humans divided into smaller populations prior to the Stone Age, and then later rejoined as a single population to repopulate the Earth and spread out to other areas.

Scientists postulate that a climatological shift, namely the series of severe droughts that hit Eastern Africa between 135, 000 and 90, 000 years ago, most probably effected these population changes, and may have led the human beings to move away from one another into smaller groups. An adviser from the Genographic Project, Paleontologist Meave Leakey, said: "Who would have thought that as recently as 70,000 years ago, extremes of climate had reduced our population to such small numbers that we were on the very edge of extinction."

The resilience of human beings at this time stands testament to our highly adaptable DNA. According to current figures held by the US Census Bureau, today more than 6.6 billion people inhabit the planet.

Anna Erian

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Picture taken from http://www.lbl.gov/Science-Articles/Archive/Genomics-Neanderthal.html
Information Sourced from http://www.news.com.au/couriermail/story/0,23739,23594665-952,00.html

Amish Lethal Microcephaly

Amish lethal microcephaly is a disorder in which infants are born with a very small head and underdeveloped brain.
Infants with Amish lethal microcephaly have an irregular forehead, jaw and chin size. The overall size of their skull is significantly smaller than a child born without the disorder. Liver problems have also been known to arise from the condition.
Affected infants are known to have difficulty maintaining their ideal body temperature and can commonly have regular seizures. The infants begin to become endowed with the effects of the conditions at around the two to three month stage of life. A compound called alpha-ketoglutaric acid can be detected in their urine and during episodes of viral illness they tend to develop elevated levels of acid in the blood and tissues. They are able to feed adequately, however their motor skills, balance and reactions to movement and sound are greatly hindered. Affected infants live only to roughly six months.

A mutation in the SLC25A19 gene causes Amish lethal microcephaly.
The SLC25A19 gene ultimately produces a protein that is a member of the solute carrier family of proteins. The protein produced from the SLC25A19 gene transports a molecule called thiamine pyrophosphate into the mitochondria. This compound is involved in the activity of a group of mitochondrial enzymes called the dehydrogenase complexes. The transport of thiamine pyrophosphate into the mitochondria is believed to be important in brain development.
All known individuals with Amish lethal microcephaly have a mutation in which the protein building block (amino acid) alanine is substituted for the amino acid glycine at position 177 of the SLC25A19 protein. Researchers believe that this mutation interferes with the transport of thiamine pyrophosphate into the mitochondria resulting in the abnormal brain development and alpha-ketoglutaric aciduria seen in Amish lethal microcephaly.
This condition is inherited in an autosomal recessive pattern. (i.e. both copies of the gene in each cell have mutations.) The parents of an individual with an autosomal recessive condition each bear one copy of the mutated gene, but do not show symptoms of the condition.