Allele frequencies in loci controlling coat colour in Polish Coldblood horses

The objective of this study was to estimate the frequencies of alleles which produce coat colour in Polish Coldblood horse population, and to verify the hypothesis that coat colour is not considered in its selection. The analysis included 35 928 horses and their parents having been registered in the studbook over a half-century. Allele frequencies in Agouti (A), Extension (E), Dun (D), Roan (Rn), and Grey (G) loci, in parental and offspring generations, were estimated according to test matings and the square root of recessive phenotype frequency. The population structure is in Hardy–Weinberg equilibrium only at E locus and coat colour is regarded by breeders. Black horses are favoured. Higher E locus homozygosity in blacks than in bays makes it easier to obtain black foals. Dun-diluted, roan and grey coat colours are undesirable and the population has come to consist almost uniformly of basic coat colours. These results show the importance of studies on population genetic structure, which despite no formal criteria for breeding for colour, can considerably change through generations.

Novel series os pea symbiotic mutants induced in the SGE line

Using ethylmethansulphonate the chemical mutagenesis of the pea laboratory line SGE was performed. During analysis of 425 families (2069 plants) of М₂ progeny 45 putative mutants were selected, among them 30 mutants forming ineffective nodules (Fix^– phenotype), 13 mutantsunable to form nodules (Nod^– phenotype), and 2 mutants forming a few nodules (Nod^+/– phenotype). For 1 Nod^– and 5 Fix^– mutants monogenic inheritance and recessive phenotype manifestation were demonstrated. For Fix^–mutant SGEFix^––9 an additional mutation leading to Nod^+/– phenotype was shown. Complementation analysis showed that the mutant phenotype of the SGEFix<span style="font-size:11px">^- - </span>5 line is caused by a mutation in the sym33 gene, of theSGEFix^––6 linein the sym40 gene, of the SGEFix^––7 line in the sym27 gene, and of the SGEFix^––8 linein the sym25 gene.

Natural Variation in the Arabidopsis Response to the Avirulence Gene hopPsyA Uncouples the Hypersensitive Response from Disease Resistance

The plant hypersensitive response (HR) is tightly associated with gene-for-gene resistance and has been proposed to function in containing pathogens at the invasion site. This tight association has made it difficult to unequivocally evaluate the importance of HR for plant disease resistance. Here, hopPsyA from Pseudomonas syringae pv. syringae 61 is identified as a new avirulence gene for Arabidopsis that triggers resistance in the absence of macroscopic HR. Resistance to P. syringae pv. tomato DC3000 expressing hopPsyA was EDS1-dependent and NDR1-independent. Intriguingly, several Arabidopsis accessions were resistant to DC3000(hopPsyA) in the absence of HR. This is comparable to the Arabidopsis response to avrRps4, but it is shown that hopPsyA does not signal through RPS4. In a cross between two hopPsyA-resistant accessions that differ in their HR response, the HR segregated as a recessive phenotype regulated by a single locus. This locus, HED1 (HR regulator in EDS1 pathway), is proposed to encode a protein whose activity can cause suppression of the EDS1-dependent HR signaling pathway. HED1-regulated symptomless gene-for-gene resistance responses may explain some cases of Arabidopsis resistance to bacteria that are classified as nonhost resistance.

Increased spontaneous DNA damage in Cu/Zn superoxide dismutase (SOD1) deficient Drosophila

The superoxide dismutases (SODs) protect oxygen-using cells against reactive oxygen species, the potentially toxic by-products of respiration, oxidative metabolism, and radiation. We have previously shown that genetic disruption of CuZn SOD (SOD1) in Drosophila imparts a recessive phenotype of reduced lifespan, infertility, and hypersensitivity to oxidative stress. We now show that the absence of SOD1 increases spontaneous genomic damage. The increase in spontaneous mutation rate occurs in SOD1-null mutants in somatic cells as well as in the germ line. Further, we show that specific DNA repair-defective mutations, which are easily tolerated in SOD1+ flies, lead to high mortality when introduced into the SOD1-null homozygous mutant background.Key words: Drosophila melanogaster, superoxide dismutase, mutations, germ and somatic cells, lethal and somatic mutations, reactive oxygen.

Tufted Is a Gain-of-Function Allele That Promotes Ectopic Expression of the Proneural Gene amos in Drosophila

The Tufted1 (Tft1) dominant mutation promotes the generation of ectopic bristles (macrochaetae) in the dorsal mesothorax of Drosophila. Here we show that Tft1 corresponds to a gain-of-function allele of the proneural gene amos that is associated with a chromosomal aberration at 36F-37A. This causes ectopic expression of amos in large domains of the lateral-dorsal embryonic ectoderm, which results in supernumerary neurons of the PNS, and in the notum region of the third instar imaginal wing, which gives rise to the mesothoracic extra bristles. Revertants of Tft1, which lack ectopic neurons and bristles, do not show ectopic expression of amos. One revertant is a loss-of-function allele of amos and has a recessive phenotype in the embryonic PNS. Our results suggest that both normal and ectopic Tft1 bristles are generated following similar rules, and both are subjected to Notch-mediated lateral inhibition. The ability of Tft1 bristles to appear close together may be due to amos having a stronger proneural capacity than that of other proneural genes like asense and scute. This ability might be related to the wild-type function of amos in promoting development of large clusters of closely spaced olfactory sensilla.