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Archive - Apr 30, 2015

Evolutionary Ancient Mechanism of Pollination by Flotation Has Been Lost in Many Conifers

A new study offers not only a sweeping analysis of how pollination has evolved among conifers, but also an illustration of how evolution -- far from being a straight-ahead march of progress -- sometimes allows for long-standing and advantageous functions to become irrevocably lost. Moreover, the authors show that the ongoing breakdown of the successful, but ultimately fragile, pollination mechanism may have led to a new diversity of traits and functions. Dr. Andrew Leslie, Assistant Professor of Ecology and Evolutionary Biology at Brown Univesity, and his co-authors studied more than 460 conifer species to order and trace the evolution of a trio of traits that provide an ancient function of pollination. Many pine and spruce species still exhibit these attributes: pollen grains that are buoyant because of structures called sacci (air-filled bladders), downward facing ovules, and the well-timed emission of a drop of liquid. For a few days a year, these trees send their pollen into the wind. The pollen grains that lands on the cone under the ovule becomes engulfed in the droplet and, because the pollen grains are buoyant, float up into the ovule. The process has the advantages of filtering out non-bouyant particles, and of guiding a concentration of pollen saccae to the otherwise well-shielded ovule. "People thought these traits were correlated," said Dr. Leslie, first author of the paper that was published online on April 22, 2015 in the journal Evolution. "What we did was put this in an evolutionary context." The article is titled “Trait integration and Macroevolutionary Patterns in the Pollination Biology of Conifers.” What the scientists found is that while the mechanism had apparently served the wide world of conifers well for hundreds of millions of years, it is gradually disappearing.

Interaction of Viral DNA and Cytoskeleton Is Ancient Evolutionary Process; Scientists Show Bacteriophages Infecting Bacteria That Lack Cytoskeleton Carry Gene for Producing Cytoskeleton Filaments to Enable Proper Trafficking of Viral DNA through the Cell

Researchers from Ludwig-Maximilians-Universitaet (LMU) in Munich, Germany have demonstrated, for the first time, that bacteriophages (bacterial viruses) carry genetic instructions for proteins that mediate the transport of their DNA to specialized replication sites in the host cell. Viruses are essentially inert nucleoprotein particles that come alive only when they find the right host cells, on which they depend for their reproduction. Bacteriophages (or “phages” for short) are viruses that infect bacteria. Work carried out by researchers led by Dr. Marc Bramkamp, who is Professor of Microbiology at LMU, and Professor Julia Frunzke at the Jülich Research Center now shows that some bacteriophages deliver certain proteins required for optimal replication of their own genomes to host cells that do not themselves possess them. The new findings were published online on April 27, 2015 in an open-access article in Nucleic Acids Research. The article is titled “A Prophage-Encoded Actin-Like Protein Required for Efficient Viral DNA Replication in Bacteria." “In order to replicate their own hereditary material, viruses must ensure that it reaches the sites of DNA replication that are normally utilized by the host and the correct egress sites where the viruses leave the host. We have now shown, for the first time, how a so-called prophage (a viral DNA that has been integrated into the genome of its host during a prior infection) organizes its own transport to such a replication site when induced to self-excise from the bacterial chromosome,” Dr. Bramkamp explains. Viruses that infect the nucleated cells of higher organisms (eukaryotes) often exploit the so-called actin cytoskeleton, a complex system of metastable fiber-like structures (filaments) for this purpose.

ITIM-Containing Receptor LAIR1 Inhibits Immune Response and Is Key to Development of Acute Myeloid Leukemia (AML); Blockade of This Signaling May Eliminate Leukemia Stem Cells and Lead to Complete Remission in AML Patients, Senior Author Suggests

University of Texas (UT) Southwestern Medical Center scientists have discovered that a certain class of receptors that inhibit the immune response are crucial for the development of acute myeloid leukemia (AML), the most common acute leukemia affecting adults. The researchers found that some receptors containing the immunoreceptor tyrosine-based inhibition motif (ITIM) are important to the development of AML, providing a new target for potential therapies. “We showed that these receptors are expressed by AML cells and that they support the development of AML. Although counterintuitive, this result is consistent with the generally immune-suppressive, and thus tumor-promoting, roles of inhibitory receptors in the immune system,” said Dr. Chengcheng “Alec” Zhang, Associate Professor of Physiology and Developmental Biology, and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. “These findings suggest that blocking ITIM-receptor signaling, in combination with conventional therapies, may represent a novel strategy for AML treatment.” AML is a type of blood and bone marrow cancer in which certain stem cells or progenitor cells fail to properly mature into healthy white blood cells and, instead, become abnormal red cells, called leukemia cells, according to the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). Leukemia cells can build up in the bone marrow and blood so there is less room for healthy white blood cells, red blood cells, and platelets, which can result in infections, anemia, or bleeding. Leukemia cells also can spread outside the blood to other parts of the body, including the central nervous system, skin, and gums, according to the NCI.