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Der Deutschen Forschungsgemeinschaft (DFG) ist WissenschaftskomZielgruppe munikation ein relevantes Anliegen. Dabei hat sie erkannt, dass KonWissenschaftsinteressierten sortien wie Sonderforschungsbereiche und Schwerpunktprogramme angeworgute Möglichkeiten bieten, aktuelle Forschung für die Öffentlichkeit transparent zu machen. Sie hat dazu Module geschaffen, mit denen anneben den wissenschaftlichen Förderanträgen - eigenständige Publicderen OutreachProjekte fnanziert werden können, die die Wissenschafts-kommunikation zur Thematik eines Konsortiums durchführen. In diesem Artikel beschreibe ich für das „CRISPRWhisper" Team, was ein solches Projekt leisten kann, aber auch was Herausforderungen sind und welche Probleme auftreten können. [ABSTRACT FROM AUTHOR]

Praktische Erfahrung durch CRISPRCasLaborexperimente erlaubt an Schulen, aber auch in der allgemeinen Öffentlichkeit bessere Einblicke in eine Methodik, die unsere Gesellschaft wesentlich beeinfussen wird. Es wurden einige einfache und sichere Experimente entwickelt, die teilweise in zwei Schulstunden durchführbar sind. Die gesetzlichen Vorgaben in Deutschland sind jedoch so restriktiv, dass selbst professionelle Schülerund Öffentlichkeitslabore zurückschrecken, den administrativen Aufwand zu wagen. Wir ermutigen die Labore, es trotzdem zu versuchen, und appellieren an die Politik, die unnötigen Hürden abzubauen. [ABSTRACT FROM AUTHOR]

Cells that overexpress PKA as a consequence of carrying multiple copies of the gene encoding the catalytic subunit can be induced to sporulate when developing as single cells. A peptide phosphorylated by PKA, termed SDF-1, has recently been shown to stimulate this process (Anjard et al., 1997). Several genes have been implicated in a signal transduction pathway by which prestalk cells induce encapsulation of prespore cells during terminal differentiation including a prestalk-specific putative membrane protease (TagC) and a two-component system consisting of a receptor-histidine kinase (DhkA) and a response regulator with cAMP phosphodiesterase activity (RegA). To determine whether SDF-1 uses this pathway, strains carrying null mutations in the pertinent genes were transformed with a pkaC plasmid such that they can overexpress PKA. Since these mutant strains all sporulated efficiently when SDF-1 was added, it appears that other gene products mediate the response. However, we found that [regA.sup.-] mutant cells release a distinct factor, SDF-2, that rapidly induces encapsulation of test cells overexpressing pkaC. Since cells in which tagC is disrupted do not form SDF-2 and cells in which dhkA is disrupted do not respond to SDF-2, this peptide appears to use the two-component system that regulates PKA activity. SDF-2 is a small peptide released by prestalk cells in a manner dependent on TagC. It appears to act on prespore cells through the DhkA receptor to inhibit the cAMP phosphodiesterase of RegA, thereby activating PKA via cAMP. The process of induction by SDF-2 can be shown to be distinct from that by SDF-1. SDF-2 appears to stimulate prestalk cells to release additional SDF-2 by acting through a signal transduction pathway that also involves DhkA, RegA, and PKA. based on these results we present a model for the signal transduction cascade regulating spore differentiation. Key Words: Dictyostelium; spore differentiation; PKA; peptide; signal transduction.

Antisense RNA has been used for some time as a versatile tool for silencing gene expression. There is ample evidence for gene regulation by endogenous antisense transcripts in prokaryotes and increasing insight into the molecular mechanisms underlying such regulation. The introduction of antisense gene constructs into eukaryotes has now become routine but the mechanisms by which gene expression is inhibited are barely understood. In recent years, several examples of endogenous eukaryotic antisense transcripts have been discovered, some of which probably serve regulatory functions. Here we will discuss a model to explain mechanisms of antisense-mediated gene silencing.