植物抗旱分子机理研究进展

干旱胁迫是影响植物生长发育的主要逆境因子之一,高等植物在长期进化过程中,逐渐演变产生了对干旱胁迫的防御机制,以最大限度减轻干旱胁迫造成的伤害。本文概述了植物耐旱生理及其分子机制。     

Genetics of early mammalian folliculogenesis

Early ovarian folliculogenesis begins with the breakdown of germ cell clusters and formation of primordial follicles. Primordial follicles are the smallest ovarian follicle units continuously recruited to grow into primary and more advanced ovarian follicles. Genes expressed in the germ cells such as Figla, Nobox, Kit and Ntrk2, as well as genes expressed in the surrounding somatic cells such as Foxl2, Kitl and Ngf, play critical functions during early folliculogenesis. Transgenic mice continue to provide important insights into the genetic pathways that regulate early mammalian folliculogenesis. Genes critical in early folliculogenesis are important determinants of reproductive life span and represent candidate genes for human ovarian failure. Received 25 August 2005; received after revision 18 October 2005; accepted 21 November 2005     

Genetics of photoreceptor degeneration and regeneration in zebrafish

Zebrafish are unique in that they provide a useful model system for studying two critically important problems in retinal neurobiology, the mechanisms responsible for triggering photoreceptor cell death and the innate stem cell–mediated regenerative response elicited by this death. In this review we highlight recent seminal findings in these two fields. We first focus on zebrafish as a model for studying photoreceptor degeneration. We summarize the genes currently known to cause photoreceptor degeneration, and we describe the phenotype of a few zebrafish mutants in detail, highlighting the usefulness of this model for studying this process. In the second section, we discuss the several different experimental paradigms that are available to study regeneration in the teleost retina. A model outlining the sequence of gene expression starting from the dedifferentiation of Müller glia to the formation of rod and cone precursors is presented.     

Genetics of sleep and sleep disorders

Genetic factors affect sleep. Studies in twin pairs demonstrate that the strong hereditary influences on sleep architecture and some sleep disorders are transmitted through families. Evidence like this strongly suggests that sleep regulation receives significant influence from genetic factors. Although recent molecular technologies have revealed evidence that genetic traits or gene products trigger particular changes in sleep electroencephalogram activity, we are still far from finding candidate genes or multiple mutations responsible for individual sleep disorders. Sleep is a very complex phenotype. Genetic susceptibility and environmental factors should be also considered as contributors to sleep phenotype. The aim of this review is to present a current summary and future prospects for genetic studies on sleep and selected sleep-associated disorders. An erratum to this article is available at .     

Genetics of toxin production and resistance in phytopathogenic bacteria

Genes for phytotoxin production have been identified and cloned from several phytopathogenic pseudomonads. These genes comprise physically linked clusters that have been located both on the chromosome and on endogenous plasmids. Contained within these genetic regions are resistance genes specific to those toxins that have a bactericidal component to their activity. DNA sequences required for toxin production are often conserved among bacteria with divergent host specificities, suggesting the ability of toxin genes to be transferred between bacteria. Toxins are usually modulators of plant pathogenicity, their production causing a significant increase in disease severity. In one case, however, toxin production appears to be a major contributor to the basic pathogenicity of a plant pathogenic bacterium.     

离体诱导单倍体在植物遗传与育种中的应用

单倍体量种特殊的生命现象,涉及到生物的起源,进化 ,胚胎发生与遗传变异等学科,受到科学家的关注。本文讨论下述问题：１）高等植物单倍体的起源;２）单倍体的遗传学;３）离体诱导单倍体的应用。     

Advances in tenascin-C biology

Tenascin-C is an extracellular matrix glycoprotein that is specifically and transiently expressed upon tissue injury. Upon tissue damage, tenascin-C plays a multitude of different roles that mediate both inflammatory and fibrotic processes to enable effective tissue repair. In the last decade, emerging evidence has demonstrated a vital role for tenascin-C in cardiac and arterial injury, tumor angiogenesis and metastasis, as well as in modulating stem cell behavior. Here we highlight the molecular mechanisms by which tenascin-C mediates these effects and discuss the implications of mis-regulated tenascin-C expression in driving disease pathology.