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Archive - Nov 15, 2014


Treasure Trove of Blind Cave Beetles Discovered in Southern China

A team of scientists specializing in cave biodiversity from the South China Agricultural University (Guangzhou) has unearthed a treasure trove of rare blind cave beetles. The description of seven new species of underground Trechinae beetles, published online on November 14, 2014 in the open-access journal ZooKeys, attests to the Du'an Karst as the most diverse area for these cave dwellers in China. "China is becoming more and more fascinating for those who study cave biodiversity, because it holds some of the most morphologically adapted cavernicolous animals in the world. This is specifically true for fishes and the threchine beetles, the second of which is also the group featured in this study," explains the senior author of the study Professor Mingyi Tian. Like most cavernicolous species, Trechinae cave beetles show a number of specific adaptations, such as lack of eyes and color, which are traits common among cave dwellers. The new Trechinae beetles belong to the genus Dongodytes, whose members are easily recognizable by their extraordinary slender and very elongated body. Members of this genus are usually very rare in caves, with only five species reported from China before now. During the recent study of the cave systems in Du'an Karst, however, this numbers drastically changed, Of the 48 visited caves, 12 held populations of trechine beetles. A total of 103 samples were collected, out of which the team of scientists determined ten different species, seven of which are new to science. "This new discovery casts a new light on the importance of the Du'an Karst as a biological hotspot for cavernicolousTrechinae in China," adds Professor Tian. Image shows a Trechinae beetle.

Scientists Discover Telomere Mechanism That Controls Fitness of Cells, Impacting Aging and Disease

A novel looping mechanism that involves the end caps of DNA may help explain the aging of cells and how they initiate and transmit disease, according to new research from University of Texas (UT) Southwestern Medical Center cell biologists. The UT Southwestern team found that the length of the endcaps of DNA, called telomeres, form loops that determine whether certain genes are turned off when young and become activated later in life, thereby contributing to aging and disease. “Our results suggest a potential novel mechanism for how the length of telomeres may silence genes early in life and then contribute to their activation later in life when telomeres are progressively shortened. This is a new way of gene regulation that is controlled by telomere length," said Dr. Jerry W. Shay, Professor and Vice Chairman of Cell Biology at UT Southwestern, who led the team with his colleague, Dr. Woodring E. Wright, Professor of Cell Biology and Internal Medicine. Telomeres cap the ends of the cell's chromosomes to protect them from damage. But the telomeres become shorter every time the cell divides. Once they shorten to a critical length, the cell can no longer divide and enters into a senescent or growth-arrest phase in which the cell produces different products compared to a young quiescent cell. Most research in this area has focused on the role that the process plays in cancer, but telomere shortening also has been shown to influence which genes are active or silent. Dr. Shay and Dr. Wright found that even before the telomeres shorten to the critical length that damages the DNA, the slow erosion in length has an effect on the cell's regulation of genes that potentially contributes to aging and the onset of disease.

New Insight into Age-Related Macular Degeneration

Scientists at The University of Manchester have identified an important new factor behind one of the major causes of blindness, which they hope could lead to new treatments. Age-related macular degeneration (AMD) is the major cause of blindness in the western world, affecting approximately 50 million people. It has been shown that sufferers are genetically predisposed to develop the condition. One of the most important risk-associated genes is called complement factor H (CFH). This encodes a protein called factor H (FH) that is responsible for protecting our eyes from attack by part of our immune system, called the complement system. FH achieves this protection by sticking to tissues, and when it is present in sufficient quantities it prevents the complement system from causing any damage. Scientists from Manchester’s Faculty of Medical and Human Sciences have now discovered that the protein factor H is not the main regulator of immunity in the back of the eye, instead it is a different protein that is made from the same CFH gene. This is called factor H-like protein 1 (FHL-1). The research was published online on October 15, 2014 in the Journal of Immunology. Dr. Simon Clark, a Medical Research Council Career Development Fellow, led the research: “FHL-1 is a smaller version of FH, in fact it is about a third of the size. However, it has all the necessary components to regulate the immune system and is still subject to the genetic alterations that affect AMD risk.

DNA Sequencing Helps Identify Mitochondrial Genetic Defects in Glaucoma

Scientists from the University of Liverpool have sequenced the mitochondrial genome in glaucoma patients to help further understanding of the genetic basis for the disease. Glaucoma is a major cause of irreversible blindness, affecting more than 60 million people worldwide, predicted to increase to an estimated 79.6 million people by 2020. It is thought that the condition has genetic origins and many experiments have shown that new sequencing approaches could help understand how the condition develops. Studies on primary open-angle glaucoma - the most common form of glaucoma - have shown that mutations in mitochondria, the energy generating structures in all cells, could give valuable insight into how to prevent the disease. Using new gene sequencing techniques, called massively parallel sequencing, the Liverpool team has produced data on the mitochondrial genome taken from glaucoma patients from around the world. The impact that mitochondrial gene change has on disease progression has been difficult to fully determine as cells in the human body can contain mixtures of healthy and mutated mitochondrial genes. Using this new technology, however, the researchers aim to support the delivery of personalized medicines to identify drugs that will target mutated mitochondria. Professor Colin Willoughby, from the University's Institute of Ageing and Chronic Disease, explains: "Understanding the genetic basis of glaucoma can direct care by helping to determine the patient's clinical risk of disease progression and visual loss. Increasing evidence suggests that mitochondrial dysfunction results in glaucoma and drugs that target mitochondria may emerge as future therapeutic interventions.