Human-specific changes of genome structure detected by genomic triangulation

Knowledge of the rhesus macaque genome sequence enables reconstruction of the ancestral state of the human genome before the divergence of chimpanzees. However, the draft quality of nonhuman primate genome assemblies challenges the ability of current methods to detect insertions, deletions, and copy-number variations between humans, chimpanzees, and rhesus macaques and hinders the identification of evolutionary changes between these species. Because of the abundance of segmental duplications, genome comparisons require the integration of genomic assemblies and data from large-insert clones, linkage maps, and radiation hybrid maps. With genomic triangulation, an integrative method that reconstructs ancestral states and the structural evolution of genomes, we identified 130 human-specific breakpoints in genome structure due to rearrangements at an intermediate scale (10 kilobases to 4 megabases), including 64 insertions affecting 58 genes. Comparison with a human structural polymorphism database indicates that many of the rearrangements are polymorphic.     

A diet-induced developmental polymorphism in a caterpillar

Caterpillars of the spring brood of Nemoria arizonaria develop into mimics of the oak catkins upon which they feed. Caterpillars from the summer brood emerge after the catkins have fallen and they develop instead into mimics of oak twigs. This developmental polymorphism may be triggered by the concentration of defensive secondary compounds in the larval diet: all caterpillars raised on catkins, which are low in tannin, developed into catkin morphs; those raised on leaves, which are high in tannin, developed into twig morphs; most raised on artificial diets of catkins with elevated tannin concentrations developed into twig morphs.     

发酵黄芪对断奶仔猪日增重、腹泻率及免疫能力的影响

将发酵黄芪添加于断奶仔猪基础日粮中,与基础日粮及抗生素作比较,研究其对断奶仔猪日增重、腹泻及免疫功能的影响。结果表明,与基础日粮组相比,发酵黄芪能显著提高仔猪日增重、降低腹泻率及免疫能力;与抗生素组相比,发酵黄芪能显著降低仔猪腹泻率,提高免疫能力。为生产新型功能饲料提供良好途径,为中药饲料添加剂替代抗生素研究奠定基础。     

In vivo footprinting of a muscle specific enhancer by ligation mediated PCR

In vivo protein-DNA interactions at the developmentally regulated enhancer of the mouse muscle creatine kinase (MCK) gene were examined by a newly developed polymerase chain reaction (PCR) footprinting procedure. This ligation mediated, single-sided PCR technique permits the exponential amplification of an entire sequence ladder. Several footprints were detected in terminally differentiated muscle cells where the MCK gene is actively transcribed. None were observed in myogenic cells prior to differentiation or in nonmuscle cells. Two footprints appear to correspond to sites that can bind the myogenic regulator MyoD1 in vitro, whereas two others represent muscle specific use of apparently general factors. Because MyoD1 is synthesized by undifferentiated myoblasts, these data imply that additional regulatory mechanisms must restrict the interaction between this protein and its target site prior to differentiation.     

Phosphatidylserine: selective enhancer of histamine release

Phosphatidylserine, in contrast with other phospholipids, markedly enhanced histamine release from rat peritoneal mast cells induced by dextran or protein antigens. This enhancing effect was selective for dextran and protein antigens and did not extend to the action of compound 48/80 or chymotrypsin. These findings suggest a role for phosphatidylserine in the response of mast cells to antigens.     

Exponential gain and saturation of a self-amplified spontaneous emission free-electron laser

Self-amplified spontaneous emission in a free-electron laser has been proposed for the generation of very high brightness coherent x-rays. This process involves passing a high-energy, high-charge, short-pulse, low-energy-spread, and low-emittance electron beam through the periodic magnetic field of a long series of high-quality undulator magnets. The radiation produced grows exponentially in intensity until it reaches a saturation point. We report on the demonstration of self-amplified spontaneous emission gain, exponential growth, and saturation at visible (530 nanometers) and ultraviolet (385 nanometers) wavelengths. Good agreement between theory and simulation indicates that scaling to much shorter wavelengths may be possible. These results confirm the physics behind the self-amplified spontaneous emission process and forward the development of an operational x-ray free-electron laser.     

Chromosomal rearrangement generating a composite gene for a developmental transcription factor

Differential gene expression in the mother cell chamber of sporulating cells of Bacillus subtilis is determined in part by an RNA polymerase sigma factor called sigma K (or sigma 27). The sigma K factor was assigned as the product of the sporulation gene spoIVCB on the basis of the partial aminoterminal amino acid sequence of the purified protein. The spoIVCB gene is now shown to be a truncated gene capable of specifying only the amino terminal half of sigma K. The carboxyl terminal half is specified by another sporulation gene, spoIIIC, to which spoIVCB becomes joined inframe at an intermediate stage of sporulation by site-specific recombination within a 5-base pair repeated sequence. Juxtaposition of spoIVCB and spoIIIC need not be reversible in that the mother cell and its chromosome are discarded at the end of the developmental cycle. The rearrangement of chromosomal DNA could account for the presence of sigma K selectively in the mother cell and may be a precedent for the generation of cell type-specific regulatory proteins in other developmental systems where cells undergo terminal differentiation.     

Control of nonapoptotic developmental cell death in Caenorhabditis elegans by a polyglutamine-repeat protein

Death is a vital developmental cell fate. In Caenorhabditis elegans, programmed death of the linker cell, which leads gonadal elongation, proceeds independently of caspases and apoptotic effectors. To identify genes promoting linker-cell death, we performed a genome-wide RNA interference screen. We show that linker-cell death requires the gene pqn-41, encoding an endogenous polyglutamine-repeat protein. pqn-41 functions cell-autonomously and is expressed at the onset of linker-cell death. pqn-41 expression is controlled by the mitogen-activated protein kinase kinase SEK-1, which functions in parallel to the zinc-finger protein LIN-29 to promote cellular demise. Linker-cell death is morphologically similar to cell death associated with normal vertebrate development and polyglutamine-induced neurodegeneration. Our results may therefore provide molecular inroads to understanding nonapoptotic cell death in metazoan development and disease.