Effectiveness of the seed wing of Pinus flexilis in wind dispersal

Limber pine ( Pinus flexilis James) seeds are usually wingless but occasionally have short, stubby wings. To determine the effectiveness of these wings in slowing seed descent, rates of fall were determined before and after wing removal. A similar experiment was conducted with seeds of Himalayan blue pine ( P. griffithii McClelland), a white pine with typically long seed wings. The short wings of limber pine seeds were found to influence rate of seed fall far less than the wings of Himalayan blue pine. This is consistent with evidence suggesting that limber pine seeds are not effectively dispersed by wind but are dependent for dispersal on Clark's Nutcracker ( Nucifraga columbiana ).        

New species of Primula (Primulaceae) from Utah

Named as a new species from the House Range of Millard County, Utah, as Primula domensis Kass & Welsh.     

Size-frequency and rank-frequency relations, power laws and exponentials: a unified approach

Power laws, such as Zipf s law, and exponential relations, leading to straight lines in logarithmic or semi-logarithmic scales, are presented in a unified setting. It is shown that the class of size-frequency power laws is larger than the class of rank-frequency power laws. Their ubiquity in all fields of science is illustrated.     

SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin

The Sir2 deacetylase regulates chromatin silencing and lifespan in Saccharomyces cerevisiae. In mice, deficiency for the Sir2 family member SIRT6 leads to a shortened lifespan and a premature ageing-like phenotype. However, the molecular mechanisms of SIRT6 function are unclear. SIRT6 is a chromatin-associated protein, but no enzymatic activity of SIRT6 at chromatin has yet been detected, and the identity of physiological SIRT6 substrates is unknown. Here we show that the human SIRT6 protein is an NAD+-dependent, histone H3 lysine 9 (H3K9) deacetylase that modulates telomeric chromatin. SIRT6 associates specifically with telomeres, and SIRT6 depletion leads to telomere dysfunction with end-to-end chromosomal fusions and premature cellular senescence. Moreover, SIRT6-depleted cells exhibit abnormal telomere structures that resemble defects observed in Werner syndrome, a premature ageing disorder. At telomeric chromatin, SIRT6 deacetylates H3K9 and is required for the stable association of WRN, the factor that is mutated in Werner syndrome. We propose that SIRT6 contributes to the propagation of a specialized chromatin state at mammalian telomeres, which in turn is required for proper telomere metabolism and function. Our findings constitute the first identification of a physiological enzymatic activity of SIRT6, and link chromatin regulation by SIRT6 to telomere maintenance and a human premature ageing syndrome.     

Functional genomic screen reveals genes involved in lipid-droplet formation and utilization

Eukaryotic cells store neutral lipids in cytoplasmic lipid droplets enclosed in a monolayer of phospholipids and associated proteins. These dynamic organelles serve as the principal reservoirs for storing cellular energy and for the building blocks for membrane lipids. Excessive lipid accumulation in cells is a central feature of obesity, diabetes and atherosclerosis, yet remarkably little is known about lipid-droplet cell biology. Here we show, by means of a genome-wide RNA interference (RNAi) screen in Drosophila S2 cells that about 1.5% of all genes function in lipid-droplet formation and regulation. The phenotypes of the gene knockdowns sorted into five distinct phenotypic classes. Genes encoding enzymes of phospholipid biosynthesis proved to be determinants of lipid-droplet size and number, suggesting that the phospholipid composition of the monolayer profoundly affects droplet morphology and lipid utilization. A subset of the Arf1-COPI vesicular transport proteins also regulated droplet morphology and lipid utilization, thereby identifying a previously unrecognized function for this machinery. These phenotypes are conserved in mammalian cells, suggesting that insights from these studies are likely to be central to our understanding of human diseases involving excessive lipid storage.     

Coherent manipulation of single spins in semiconductors

During the past few years, researchers have gained unprecedented control over spins in the solid state. What was considered almost impossible a decade ago, in both conceptual and practical terms, is now a reality: single spins can be isolated, initialized, coherently manipulated and read out using both electrical and optical techniques. Progress has been made towards full control of the quantum states of single and coupled spins in a variety of semiconductors and nanostructures, and towards understanding the mechanisms through which spins lose coherence in these systems. These abilities will allow pioneering investigations of fundamental quantum-mechanical processes and provide pathways towards applications in quantum information processing.     

Passenger deletions generate therapeutic vulnerabilities in cancer

Inactivation of tumour-suppressor genes by homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighbouring genes. We propose that homozygous deletions in such passenger genes can expose cancer-specific therapeutic vulnerabilities when the collaterally deleted gene is a member of a functionally redundant family of genes carrying out an essential function. The glycolytic gene enolase 1 (ENO1) in the 1p36 locus is deleted in glioblastoma (GBM), which is tolerated by the expression of ENO2. Here we show that short-hairpin-RNA-mediated silencing of ENO2 selectively inhibits growth, survival and the tumorigenic potential of ENO1-deleted GBM cells, and that the enolase inhibitor phosphonoacetohydroxamate is selectively toxic to ENO1-deleted GBM cells relative to ENO1-intact GBM cells or normal astrocytes. The principle of collateral vulnerability should be applicable to other passenger-deleted genes encoding functionally redundant essential activities and provide an effective treatment strategy for cancers containing such genomic events.