World's Largest Coral Reef System Offers a Clue to Development of a Super Sunscreen

It was amazing to study the way the reef's corals protect themselves from ultraviolet light for millions of years. Scientists found the presence of natural filters which keep away the damaging rays.

Researchers came out with a safe and powerful sunscreen which can protect against harmful UV radiation which causes sunburn and skin cancer.

"The filters are clear in colour, virtually odourless and very stable, which makes them easy to be incorporated into any emulsion," said scientist Dr Mark York.

Scientists hope that the sunscreen will be available globally within five years.

Source-Medindia

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Vitamin C's Influence on Stem Cells Key to Normal Development in Mice

The study led by UC San Francisco researchers found that vitamin C assists enzymes that play a crucial role in releasing the brakes that keep certain genes from becoming activated in the embryo soon after fertilization, when egg and sperm fuse.

The discovery might eventually lead to the use of vitamin C to improve results of in vitro fertilization, in which early embryos now are typically grown without the vitamin, and also to treat cancer, in which tumor cells abnormally engage or release these brakes on gene activation, the researchers said.

In the near term, stem-cell scientists may begin incorporating vitamin C more systematically into their procedures for growing the most healthy and useful stem cells, according to UCSF stem-cell scientist Miguel Ramalho-Santos, PhD, who led the study.

In fact, the unanticipated discovery emerged from an effort to compare different formulations of the growth medium, a kind of nutrient broth used to grow mouse embryonic stem cells in the lab.

Rather than building on any previous body of scientific work, the identification of the link between vitamin C and the activation of genes that should be turned on in early development was serendipitous, Ramalho-Santos said.

Working in Ramalho-Santos' lab, graduate student Kathryn Blaschke and postdoctoral fellow Kevin Ebata, PhD, were comparing different commercial growth media for mouse stem cells. The researchers began exploring how certain ingredients altered gene activity within the stem cells. Eventually they discovered that adding vitamin C led to increased activity of key enzymes that release the brakes that can prevent activation of an array of genes.

The brakes on gene activation that vitamin C helps release are molecules called methyl groups. These methyl groups are added to DNA at specific points along the genome to prevent specific genes from getting turned on.

During the development of multicellular organisms, humans among them, different patterns of methylation arise in different cells as methyl groups are biochemically attached to DNA at specific points along the genome during successive cell divisions. Normally this gradual methylation, a key part of the developmental program, is not reversible.

But after fertilization and during early development, a class of enzymes called "Tet" acts on a wide array of the methyl groups on the DNA to remove these brakes, so that genes can be activated as needed.

The UCSF researchers demonstrated that Tet enzymes require vitamin C for optimal activity as they act to remove the methyl groups from the DNA and to stimulate gene activity that more faithfully mimics in cultured stem cells what occurs at early stages of development in the mouse embryo.

"Potential roles for vitamin C in the clinic - including in embryo culture media used during in vitro fertilization, which currently do not contain vitamin C, and in cancers driven by aberrant DNA methylation - deserve exploration," Ramalho-Santos, said.

The study is published in the journal Nature.

Source-ANI

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Genes Involved in Birth Defects Linked to Development of Mental Illness

Over the past several years, researchers in the laboratory of psychiatrist Benjamin Cheyette, MD, PhD, have shown that mice with mutations in a gene called Dact1 are born with a range of severe malformations, including some reminiscent of spina bifida in humans.

In a new study designed to explore whether Dact1 mutations exert more nuanced effects in the brain that may lead to mental illness, Cheyette, John Rubenstein, MD, PhD, and colleagues in UCSF's Nina Ireland Laboratory of Developmental Neurobiology used a genetic technique in mice to selectively delete the Dact1 protein only in interneurons, a group of brain cells that regulates activity in the cerebral cortex, including cognitive and sensory processes. Poor function of interneurons has been implicated in a range of psychiatric conditions.

As reported in the June 24, 2013 online issue of PLOS ONE, when the research team examined these genetically altered interneurons in adult mice, they found that the cells appeared relatively normal and had managed to find their proper position in the brain's circuitry during development. But the cells had significantly fewer synapses, the sites where communication with neighboring neurons takes place. In additional observations not included in the new paper, the team also noted that the cells' dendrites, fine extensions that normally form bushy arbors studded with synapses, were poorly developed and sparsely branched.

"When you delete this gene function after initial, early development -- just eliminating it in neurons after they've formed -- they migrate to the right place and their numbers are correct, but their morphology is a little off," Cheyette said. "And that's very much in line with the kinds of pathology that people have been able to identify in psychiatric illness. Neurological illnesses tend to be focal, with lesions that you can identify or pathology you can see on an imaging study. Psychiatric illnesses? Not so much. The differences are really subtle and hard to see."

The Dact1 protein is part of a fundamental biological system known as the Wnt (pronounced "wint") signaling pathway. Interactions among proteins in the Wnt pathway orchestrate many processes essential to life in animals as diverse as fruit flies, mice, and humans, including the proper development of the immensely complex human nervous system from a single fertilized egg cell.

One way the Wnt pathway manages this task is by maintaining the "polarity" of cells during development, said Cheyette, "a process of sequestering, increasing the concentration of one set of proteins on one side of the cell and a different set of proteins on the other side of the cell." Polarity is particularly important as precursor cells transform into nerve cells, Cheyette said, because neurons are "the most polarized cells in the body," with specialized input and output zones that must wind up in the proper spots if the cells are to function normally.

Cheyette said his group is now conducting behavioral experiments with the mice analyzed in the new PLOS ONE paper and with genetically related mouse lines to test whether these mice have behavioral abnormalities in sociability, sensory perception, anxiety, or motivation that resemble symptoms in major psychiatric disorders. He also hopes to collaborate with UCSF colleagues on follow-up experiments to determine whether the activity of neurons lacking Dact1 is impaired in addition to the structural flaws identified in the new study and prior published work from his lab.

Meanwhile, as yet unpublished findings from human genetics research conducted by Cheyette's group suggest that individuals with autism are significantly more likely than healthy comparison subjects to carry mutations in a Wnt pathway gene called WNT1.

"Just because a gene plays an important role in the embryo doesn't mean it isn't also important in the brain later, and might be involved in psychiatric pathology," said Cheyette. "When these genes are mutated, someone may look fine, develop fine, and have no obvious medical problems at birth, but they may also develop autism in childhood or have a psychotic break in adulthood and develop schizophrenia."

Rubenstein is the Nina Ireland Distinguished Professor in Child Psychiatry.

Source-Eurekalert

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