The human genome project: Towards an analysis of the empirical,ethical, and conceptual issues involved

In this paper I claim that the goal of mapping and sequencing the human genome is not wholly new, but rather is an extension of an older project to map genes, a central aim of genetics since its birth. Thus, the discussion about the value of the HGP should not be posed in global terms of acceptance or rejection, but in terms of how it should be developed. The first section of this paper presents a brief history of the project. The second section distinguishes among four kinds of issues relevant to an evaluation of the HGP: those economic and organizational issues related to the feasibility of the project; the ethical questions arising in the development of the project and the application of the data gathered; the empirical issues relevant to the scientific value of the project; and conceptual issues like reductionism and determinism relevant to understand the nature and scope of the project. In a third section, I analyze in detail whether the HGP and, more generally, molecular biology is reductionistic.     

Agar fractions could protect apple shoots cultured in liquid media against hyperhydricity

Apple shoots were grown in a Murashige and Skoog liquid proliferation medium containing 4.4 10 -6 M BA, and supplemented with various fractions of agar. Hydrolysed agar from Difco was able to overcome hyperhydricity when its concentration was increased to 0.7%. Among the fractions isolated from this hydrolysed agar, only oligosaccharides were found to reduce the occurrence of this developmental abnormality. The most anti-hyperhydric fraction had a molecular weight slightly less than 1900 daltons and contained methylated and sulphated galactose derivatives. This revised version was published online in June 2006 with corrections to the Cover Date.     

Wirkung von Fungiziden auf die Sporulation von Podosphaera leucotricha (Ell. et Ev.) Salm. und Venturia inaequalis (Cooke) Wint

This paper presents the results of 3 year‐long monitoring of crop fields in four ecologically different areas of Ukraine for several phytoviral infections. Various modifications of ELISA were used as main assay to evaluate the spreading of a virus. The technique allowing to determine the frequency of occurrence for a virus of interest is proposed. This technique is based on an identification of viral antigens in crops, accompanying weeds and soil. The differences between the investigated regions on a virus occurrence frequency as well as dynamics of the parameter in relation to crop‐rotation have been revealed. The possibility to use results obtained for predicting phytoviral disease spreading is discussed.     

Inhibiting autophagy reduces retinal degeneration caused by protein misfolding

Mutations in the genes necessary for the structure and function of vertebrate photoreceptor cells are associated with multiple forms of inherited retinal degeneration. Mutations in the gene encoding RHO (rhodopsin) are a common cause of autosomal dominant retinitis pigmentosa (adRP), with the Pro23His variant of RHO resulting in a misfolded protein that activates endoplasmic reticulum stress and the unfolded protein response. Stimulating macroautophagy/autophagy has been proposed as a strategy for clearing misfolded RHO and reducing photoreceptor death. We found that retinas from mice heterozygous for the gene encoding the RHO^P23H variant (hereafter called P23H) exhibited elevated levels of autophagy flux, and that pharmacological stimulation of autophagy accelerated retinal degeneration. In contrast, reducing autophagy flux pharmacologically or by rod-specific deletion of the autophagy-activating gene Atg5, improved photoreceptor structure and function. Furthermore, proteasome levels and activity were reduced in the P23H retina, and increased when Atg5 was deleted. Our findings suggest that autophagy contributes to photoreceptor cell death in P23H mice, and that decreasing autophagy shifts the degradation of misfolded RHO protein to the proteasome and is protective. These observations suggest that modulating the flux of misfolded proteins from autophagy to the proteasome may represent an important therapeutic strategy for reducing proteotoxicity in adRP and other diseases caused by protein folding defects.