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Archive - Jan 4, 2014

Mating Observed for First Time in Sleeping Sickness Parasites

Caught in the act! Researchers from the University of Bristol in the UK have observed mating for the first time in the microbes responsible for African sleeping sickness. This tropical disease is caused by trypanosomes, single-celled parasites that are found in the blood of those afflicted. The Bristol team was able to see what the trypanosomes were doing inside the tsetse flies that carry the disease by using fluorescent markers. The microscopic parasites were seen twirling and gyrating together before joining up into one hybrid cell. To tell which was which, individual trypanosomes were tagged with different colors, with the result that the hybrid cells had both colours. Professor Wendy Gibson, who led the research, commented: “It’s not only bigger animals that have intricate courtship – but you need a powerful microscope to see this!” Sex matters for microbes because it enables genes to be swapped between different strains, leading to new combinations of genes. In the case of disease-causing microbes like the trypanosome, sex can potentially lead to a lot of harmful genes being combined in one strain. These new results suggest that sex is not an optional or rare part of this microbe’s life cycle, but probably happens every time two different trypanosomes find themselves together in the same tsetse fly. Trypanosomes (see image) belong to a strange group of protozoa that includes several other medically important parasites such as Leishmania, Trichomonas, and Giardia. In the past, all these microbes were thought to reproduce just by splitting in half, but now results show that they also use sex to swap genes between strains.

Loss of Function of Singe Gene Causes Type 2 Diabetes in Mice

Researchers from the University of Illinois at Chicago (UIC) College of Medicine have found that dysfunction in a single gene in mice causes fasting hyperglycemia, one of the major symptoms of type 2 diabetes. Their findings were reported online on December 30, 2013 in the journal Diabetes. If a gene called MADD (which codes for MAP kinase-activating death domain protein) is not functioning properly, insulin is not released into the bloodstream to regulate blood sugar levels, says Dr. Bellur S. Prabhakar, professor and head of microbiology and immunology at UIC and lead author of the paper. Type 2 diabetes affects roughly 8 percent of Americans and more than 366 million people worldwide. It can cause serious complications, including cardiovascular disease, kidney failure, loss of limbs and blindness. In a healthy person, beta cells in the pancreas secrete the hormone insulin in response to increases in blood glucose after eating. Insulin allows glucose to enter cells where it can be used as energy, keeping glucose levels in the blood within a narrow range. People with type 2 diabetes don’t produce enough insulin or are resistant to its effects. They must closely monitor their blood glucose throughout the day and, when medication fails, inject insulin. In previous work, Dr. Prabhakar isolated several genes from human beta cells, including MADD, which is also involved in certain cancers. Small genetic variations found among thousands of human subjects revealed that a mutation in MADD was strongly associated with type 2 diabetes in Europeans and Han Chinese. People with this mutation had high blood glucose and problems of insulin secretion – the “hallmarks of type 2 diabetes,” Dr. Prabhakar said.