Syndicate content

Archive - Mar 11, 2015

Hemocyanin Helps Arctic Octopus Survive Frigid Temperatures

An Antarctic octopus that lives in ice-cold water uses an unique strategy to transport oxygen in its blood, according to research published in Frontiers in Zoology. The study suggests that the octopus's specialized blood pigments could help to make it more resilient to climate change than Antarctic fish and other species of octopus. The Antarctic Ocean hosts rich and diverse fauna despite inhospitable temperatures close to freezing. While it can be hard to deliver oxygen to tissues in the cold due to lower oxygen diffusion and increased blood viscosity, ice-cold waters already contain large amounts of dissolved oxygen. In Antarctic fish, this reduces the need for active oxygen transport by blood pigments (e.g., haemoglobin), but little is known about the adaptations employed by blue-blooded octopods to sustain oxygen supply in the cold. Lead author Dr. Michael Oellermann from the Alfred-Wegener-Institute, in Germany, said: "This is the first study providing clear evidence that the octopods' blue blood pigment, hemocyanin, undergoes functional changes to improve the supply of oxygen to tissue at sub-zero temperatures. This is important because it highlights a very different response compared to Antarctic fish to the cold conditions in the Southern Ocean. The results also imply that due to improved oxygen supply by hemocyanin at higher temperatures, this octopod may be physiologically better equipped than Antarctic fishes to cope with global warming." Octopods have three hearts and contractile veins that pump “hemolymph,” which is highly enriched with the blue oxygen transport protein hemocyanin (analogous to hemoglobin in vertebrates).

Surprise Link Between Weaning and Beta Cell Maturation Is Important for Diabetes, Cell Regeneration

A long-standing puzzle in the diabetes field has been the fact that only a small subset of insulin-producing beta cells in the pancreas of adult organisms can replicate (and, hence, contribute to beta cell regeneration in diabetes). Furthermore, this subset of replicating cells continues to decline with advancing age. Young animals demonstrate a superb potential for tissue regeneration. Because this tissue regeneration deteriorates with age, it is generally assumed that the younger the animal, the better it compensates for tissue damage. In a new study published in Developmental Cell, Professor Yuval Dor and research associate Dr. Miri Stolovich-Rain at the Hebrew University of Jerusalem’s Institute for Medical Research Israel-Canada (IMRIC), in collaboration with Professor Benjamin Glaser from the Hadassah Medical Center, set out to understand the age-related decline of beta cell regeneration. To do this, they examined the ability of beta cells in young mice to replicate in response to hyperglycemia, a condition in which excessive glucose circulates in the blood. Expecting to find a superb regenerative response that declines with age, the researchers were surprised to discover that young mice don’t begin to possess the cellular machinery that allows them to regenerate after they are done weaning. Examining the production of pancreatic beta cells in suckling mice, the researchers found that in these young mice, beta cells failed to enter the cell division cycle in response to high levels of glucose. In addition, insulin secretion in response to high levels of glucose was much reduced compared with the situation in adult mice.

Toll-Like Receptors Fine-Tune Immune Response

Microbiologists at the University of British Columbia (UBC) have uncovered a novel mechanism that boosts B-cells’ sensitivity to extremely small amounts of foreign molecules. The immune system typically combines signals from B-cell antigen receptors (which distinguish foreign molecules) and Toll-like receptors (which recognize common microbial components) to mount responses. But the new work indicates that the Toll-like receptors are able to pre-emptively initiate changes in the B-cell’s structure to kick-start the antigen receptors' activity. The findings could inform vaccine design, and may explain the molecular basis for certain autoimmune diseases and B cell malignancies. When microbial molecules bind to Toll-like receptors, filaments underlying the B cell’s plasma membrane break apart. This allows B-cell antigen receptors, normally confined to compartments by the filaments, to move more freely within the membrane. “The increase in B-cell antigen receptor mobility and collisions at the membrane initiates signaling to the inside of the cell, even in the absence of antigen,” says UBC microbiologist Dr. Mike Gold, lead author on the paper published online on February 3, 2015 in Nature Communications. The paper was titled “Toll-Like Receptor Ligands Sensitize B-Cell Receptor Signalling by Reducing Actin-Dependent Spatial Confinement of the Receptor.” “So maximum signaling can now be induced by much smaller amounts of antigen than in cells that have not been exposed to microbial components.” The study was a collaboration among Dr. Gold, UBC mathematician Dr. Dan Coombs, and UBC Cellular and Physiological Sciences’ Dr. Cal Roskelley. Dr. Coombs and former UBC post-doc Dr. Raibatak Das performed mathematical analyses that quantitatively characterized how TLR signaling altered antigen receptor mobility within the cell membrane.

Seychelles Palm Tree Creates Highly Fertile Environment at Its Base

Tourists are familiar with the Lodoicea maldivica palm, also called coco de mer, mainly because of their bizarrely shaped fruits and because the plant produces the world’s largest known seed. Scientists, however, are fascinated by the huge plants – which are abundant on the Seychelles islands of Praslin and Curieuse – for entirely different reasons. The coco de mer palm engages in a lot of effort for reproduction, producing large amounts of pollen and huge fruits that cannot be spread around, but rather fall to the ground at the base. “This is an enormous commitment of energy in very nutrient-poor soil – it does not really make sense,” says Dr. Christopher Kaiser-Bunbury of the Department of Biology at TU Darmstadt, Germany, describing the contradiction that brought about the study by a group of researchers from the Swiss Federal Institute of Technology in Zurich, the Seychelles Islands Foundation, and TU Darmstadt. “We asked ourselves how these palms get the nutrients they need for this.” The study of the slow-growing coco de mer palm trees in the UNESCO Heritage Site Vallée de Mai on Praslin took several years. The scientists measured the amounts of phosphate and nitrogen that the palms invest into reproduction and growth, the amount available of these nutrients in the soil, the amount of water that flowed down the palm trunk during rain showers, as well as soil moisture in certain areas around the plants. The researchers found that the special leaves of the coco de mer palm play a particular role. The broad, slightly feathery leaves reach enormous size – sometimes up to 10 square meters – and have a funnel shape, forming a tube that goes down the trunk. As a result, the palm captures water as well as animal and plant organic waste and debris.

KCNA2 Ion Channel Gene Linked to Early Forms of Epilepsy

Certain types of early-onset epilepsy are caused by previously unknown mutations of a potassium channel gene, KCNA2. The mutations disrupt the electrical balance in the brain in two ways. In some patients, the flow of potassium is greatly reduced; while in others, it is raised enormously. Both states can lead to hard-to-treat epileptic seizures. Mental and motor development can come to a stop, or even regress. These findings were made by a group of European scientists led by researchers at the Universities of Leipzig and Tübingen in Germany. Their results were published online on March 9, 2015 in Nature Genetics. The article is titled “De Novo Loss- or Gain-of-Function Mutations in KCNA2 Cause Epileptic Encephalopathy.” Among what the brain needs in order to function is the interaction of many different ion channels, which regulate electrical signals by keeping a delicate balance between the influences which make cells rest or become excited. The ion channels are located in the cell wall of a neuron, together with many other pores and channels. “The potassium channel KCNA2 is one of many channels. It regulates the flow of potassium ions by opening and shutting, thereby also regulating the electrical excitability of the neurons in the brain,” explains Professor Johannes Lemke, head of Leipzig University Hospitals’ Institute of Human Genetics. Mutations in various ion channels are one of the main causes of epilepsy. “That is why identifying each mutation in the ion channel is important for diagnosing the individual epilepsy syndrome and finding ways of treating it,” says Professor Holger Lerche, of Tübingen’s Hertie Institute for Clinical Brain Research (HIH) and medical director of Neurology and Epileptology at the Tübingen University Hospitals.

Using Single-Cell Transcriptogenonomics, Scientists Demonstrate Powerful Cellular Mechanism to Prevent Transcription of Newly Mutated DNA

The central dogma of molecular biology describes the flow of genetic information. It was first described by Dr. Francis Crick in 1956 as one-way traffic: as: "DNA makes RNA and RNA makes protein." A recent open-access paper published in the February 2015 issue of Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, however suggests that, rather than being a one-way street, DNA-directed RNA transcription may have profound adaptability. The paper is titled “"Single-cell Transcriptogenomics Reveals Transcriptional Exclusion of ENU-mutated Alleles." The authors of the paper showed a conceptually novel relationship between the genotype (DNA) and the phenotype (the products of the transcription of DNA). The method the authors used to make this discovery is termed Single-Cell Transcriptogenomics (SCTG). It allows DNA and RNA sequencing to be performed concurrently on the same single cells taken from a cell population treated with the powerful mutagen ethylnitrosourea. This method allowed the authors, for the first time, to prove the tendency of the transcriptional machinery in the cell to avoid transcribing DNA strands harboring a newly induced mutation. This is likely to be a novel cellular defense mechanism to prevent genetic mutations from being expressed. "We described a novel method to directly examine the transcription pattern of genotypic variants at single cell resolution," explained Dr. Jan Vijg, Department of Genetics, Albert Einstein College of Medicine, lead author of the paper. "Single-cell transcriptogenomics will be instrumental in gaining a more complete understanding of how variations in the genome can lead to functional deficiencies in aging and disease."