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In the 18th and 19th century crossing experiments using maize, ornamentals and peas were carried out in Europe and in the USA. Mendel knew at least a part of the literature when he published his famous paper "Experiments on Plant Hybridisation" with the original German title "Versuche über Pflanzenhybriden" in 1866. In contrast to his predecessors, Mendel recognised the constant segregation ratios appearing in the progenies of the crossings. After being unnoticed for decades, his fundamental theory of heredity was rediscovered and experimentally verified by de Vries, Correns and Tschermak in 1900. Shortly after the English translation of Mendel's work became available in 1901, Raphael Weldon, one of the founders of biometry, published his doubts on Mendel's data since all observed segregation ratios were extremely close to the expected ones. Ronald A. Fisher concluded in a paper from 1936 that a large part of Mendel's results must have been falsified to agree closely with the postulated segregation ratios. The Mendel-Fisher controversy was born. In 1966, 100 years after Mendel's original paper was released, Stern & Sherwood published a book comprising translations of Mendel's laws of inheritance, the rediscovery by de Vries and Correns and Fisher's paper. Subsequently, this led to the publication of numerous articles from different scientific disciplines on the Mendel-Fisher controversy. It may never be revealed, if it was simple luck, if Mendel sorted out plants, which did not represent the theory, or if he had an assistant "who knew too well what was expected", as Fisher speculated in 1936. Nonetheless, Mendel's work doubtlessly culminated in one of the most important breakthrough discoveries of the 19th century and is the starting point of modern genetics and plant breeding. [ABSTRACT FROM AUTHOR]

In this study, Brassica rapa subsp. rapifera (ECD 02) which exhibits broad-spectrum resistance to many Canadian Plasmodiophora brassicae isolates was crossed with two clubroot-susceptible B. rapa accessions to produce two F2 populations. The F2 plants were screened against P. brassicae pathotypes 3H, 5X, and 5G. The Chi-square goodness of fit test showed that the vast majority (≈75%) of the crosses that produced the F2 populations showed segregation ratios of 9R:7S, 7R:9S, 13R:3S, 3R:13S, 5R:11S, 11R:5S, and 1R:15S. These were modifications of the 15R:1S ratio expected for the inheritance of two dominant major clubroot resistance (CR) genes from ECD 02. The distorted segregation ratios suggest that the two resistance genes are on different chromosomes and that two genes interact in an epistatic manner to confer resistance. Genotyping was conducted with 144 PCR-based markers in the two F2 populations. Linkage and QTL analysis with the polymorphic markers identified two QTLs on chromosome A03 to be associated with resistance to P. brassicae pathotypes 5X and 5G in Popl#1 while only the second QTL on chromosome A03 was associated with resistance to pathotypes 5X and 5G in Popl#2. The QTLs clustered in genomic regions on the A03 chromosome of B. rapa where the CRa/CRbKato gene(s) are mapped. In addition, the Crr1 gene on the A08 chromosome of B. rapa was detected in the two F2 populations. Therefore, the phenotypic and molecular data confirm the existence of two CR genes in ECD 02. This is the first study that shows that major dominant genes in Brassica interact in a non-additive manner to confer resistance to different P. brassicae pathotypes.Key Message: This study provides knowledge on the inheritance and type of gene action for clubroot resistance derived from Brassica rapa subsp. rapifera (ECD 02). The results indicated that duplicate recessive and recessive suppression epistatic interactions, digenic additivity and complementary gene action between the CRa/CRbKato gene(s) on the A03 and the Crr1 gene on the A08 chromosome of B. rapa controlled clubroot resistance to P. brassicae pathotypes 3H, 5X and 5G.

In this study, Brassica rapa subsp. rapifera (ECD 02) which exhibits broad-spectrum resistance to many Canadian Plasmodiophora brassicae isolates was crossed with two clubroot-susceptible B. rapa accessions to produce two F 2 populations. The F 2 plants were screened against P. brassicae pathotypes 3H, 5X, and 5G. The Chi-square goodness of fit test showed that the vast majority (≈75%) of the crosses that produced the F 2 populations showed segregation ratios of 9R:7S, 7R:9S, 13R:3S, 3R:13S, 5R:11S, 11R:5S, and 1R:15S. These were modifications of the 15R:1S ratio expected for the inheritance of two dominant major clubroot resistance (CR) genes from ECD 02. The distorted segregation ratios suggest that the two resistance genes are on different chromosomes and that two genes interact in an epistatic manner to confer resistance. Genotyping was conducted with 144 PCR-based markers in the two F 2 populations. Linkage and QTL analysis with the polymorphic markers identified two QTLs on chromosome A03 to be associated with resistance to P. brassicae pathotypes 5X and 5G in Popl#1 while only the second QTL on chromosome A03 was associated with resistance to pathotypes 5X and 5G in Popl#2. The QTLs clustered in genomic regions on the A03 chromosome of B. rapa where the CRa / CRb Kato gene(s) are mapped. In addition, the Crr1 gene on the A08 chromosome of B. rapa was detected in the two F 2 populations. Therefore, the phenotypic and molecular data confirm the existence of two CR genes in ECD 02. This is the first study that shows that major dominant genes in Brassica interact in a non-additive manner to confer resistance to different P. brassicae pathotypes. Key Message: This study provides knowledge on the inheritance and type of gene action for clubroot resistance derived from Brassica rapa subsp. rapifera (ECD 02). The results indicated that duplicate recessive and recessive suppression epistatic interactions, digenic additivity and complementary gene action between the CRa / CRb Kato gene(s) on the A03 and the Crr1 gene on the A08 chromosome of B. rapa controlled clubroot resistance to P. brassicae pathotypes 3H, 5X and 5G. [ABSTRACT FROM AUTHOR]

Nutritious and functional foods from wheat have received great attention in recent years. Colored-grain wheat contains a large number of nutrients such as anthocyanins and hence the breeding is interesting. In this work, colored-grained wheat lines of mixed pollination of einkorn wheat (Triticum boeoticum, AA) and French rye (French Secale cereale, RR) were used as male parents and wheat line Y1642 (derived from common wheat and Agropyron elongatum, AABBDD) was used as the female parent. These colored wheat were used for diallel cross to study the segregation ratios of F1 colored grains. Results show that the color inheritance of purple-grained wheat follows a maternal inheritance pattern and that the blue-grained wheat expresses xenia in most cases. In some circumstances, the grains with different color shades appear in the same spike.

Turnip mosaic virus (TuMV) causes a damaging disease in Brassica juncea, an important oilseed and biofuel crop. B. juncea gene TuRBJU 01 is associated with a systemic hypersensitive phenotype in TuMV-infected plants. Plants of TuMV-susceptible parent JM 06006, TuMV-resistant parent Oasis Cl (which carries TuRBJU 01) and F3 progeny plants obtained by crossing them were inoculated with 10 Australian TuMV isolates, most of which were already pathotyped. These were: NSW-1, NSW-5 (pathotype 7), NSW-2, NSW-6 (pathotype 1), WA-Ap, WA-Ap1 (pathotype 8), NSW-3, NSW-4 (new pathotype) and 12.1 and 12.5 (unpathotyped B. napus resistance breaking isolates). JM 06006 plants developed a susceptible phenotype with all isolates while a systemic hypersensitive phenotype resulted with all isolates except NSW-3 in Oasis Cl plants. With seven isolates, the segregation ratios for necrotic: non-necrotic phenotypes obtained in inoculated F3 progeny plants all fitted a 3:1 ratio. However, with isolates 12.5 and 12.1, although pooled test segregation data did not fit a 3:1 ratio, individual test data sometimes did. Thus, TuRBJU 01 was less effective against 12.1 and 12.5, and overcome by NSW-3. Also, phenotypic responses obtained with TuRBJU 01 were unrelated to those of TuMV resistance genes present in B. napus differentials. TuRBJU 01 will be valuable in breeding TuMV-resistant B. juncea cultivars. [ABSTRACT FROM AUTHOR]

Background: Fatty acid composition of oil extracted from peanut (Arachis hypogaea L.) seed is an important quality trait because it may affect the flavor and shelf life of resulting food products. In particular, a high ratio of oleic (C18:1) relative to linoleic (C18:2) fatty acid (O/L ⩾ 10) results in a longer shelf life. Previous reports suggest that the high oleic (~80%) trait was controlled by recessive alleles of ahFAD2A and ahFAD2B, the former of which is thought to have a high frequency in US runner- and virginia-type cultivars. Functional mutations, G448A in ahFAD2A and 442insA in ahFAD2B eliminate or knock down desaturase activity and have been demonstrated to produce peanut oil with high O/L ratios. In order to employ marker assisted selection (MAS) to select a high oleic disease resistant peanut and to evaluate genotypic and phenotypic variation, crosses were made between high oleic (~80%) and normal oleic (~50%) peanuts to produce segregating populations. Results: A total of 539 F2 progenies were randomly selected to empirically determine each ahFAD2 genotype and the resulting fatty acid composition. Five of the six crosses segregated for the high oleic trait in a digenic fashion. The remaining cross was consistent with monogenic segregation because both parental genotypes were fixed for the ahFAD2A mutation. Segregation distortion was significant in ahFAD2A in one cross; however, the remaining crosses showed no distortion. Quantitative analyses revealed that dominance was incomplete for the wild type allele of ahFAD2, and both loci showed significant additive effects. Oleic and linoleic acid displayed five unique phenotypes, based on the number of ahFAD2 mutant alleles. Further, the ahFAD2 loci did exhibit pleiotropic interactions with palmitic (C16:0), oleic (C18:1), linoleic (C18:2) acids and the O/L ratio. Fatty acid levels in these progeny were affected by the parental genotype suggesting that other genes also influence fatty acid composition in peanut. As far as the authors are aware, this is the first study in which all of the nine possible ahFAD2 genotypes were quantitatively measured. Conclusions: The inheritance of the high oleic trait initially was suggested to be controlled by dominant gene action from two homoeologous genes (ahFAD2A and ahFAD2B) exhibiting complete recessivity. Analyzing the ahFAD2 genotypes and fatty acid compositions of these segregating peanut populations clearly demonstrated that the fatty acid contents are quantitative in nature although much of the variability in the predominant fatty acids (oleic, linoleic, and palmitic) is controlled by only two loci. [ABSTRACT FROM AUTHOR]

Abstract: Genetic and kernel texture relationships between Puroindoline b-2 variants 2 and 3 have not been fully established in wheat (Triticum aestivum L.). Here, 480 F2 plants, derived from three hard spring wheat populations were used to test the segregation of Puroindoline b-2 (Pinb-2) variants 2 and 3. Chi-square analysis indicated that Pinb-2 variants 2 and 3 in all three F2 populations segregated as a single bi-allelic locus, with segregation ratios fitting a 1:2:1 ratio. Using 448 of the 480 plants derived from these three F2 populations, the average SKCS hardness index of plants homozygous for Pinb-2 variant 2 vs. those homozygous for variant 3 was not significantly different (67.5 vs. 67.9). Results indicated that plants with Pina-D1b/Pinb-D1a were on average 10.0 Single Kernel Characterization System (SKCS) hardness index units harder than those carrying the Pina-D1a/Pinb-D1b haplotype. In conclusion, Pinb-2 variants 2 and 3 are allelic and exert little effect on kernel texture in hard-kernel T. aestivum germplasm. Further, the designation of Pinb-2v2 and Pinb-2v3 should be changed to Pinb-B2a and Pinb-B2b, respectively. We propose that Pinb-2 variants 1 and 4 of Chinese Spring be designated Pinb-D2a and Pinb-A2a, respectively. [Copyright &y& Elsevier]

Nutritious and functional foods from wheat have received great attention in recent years. Colored-grain wheat contains a large number of nutrients such as anthocyanins and hence the breeding is interesting. In this work, colored-grained wheat lines of mixed pollination of einkorn wheat (Triticum boeoticum, AA) and French rye (French Secale cereale, RR) were used as male parents and wheat line Y1642 (derived from common wheat and Agropyron elongatum, AABBDD) was used as the female parent. These colored wheat were used for diallel cross to study the segregation ratios of F1 colored grains. Results show that the color inheritance of purple-grained wheat follows a maternal inheritance pattern and that the blue-grained wheat expresses xenia in most cases. In some circumstances, the grains with different color shades appear in the same spike. [ABSTRACT FROM AUTHOR]

The coat protein (CP) gene of potato leafroll luteovims (PLRV) was inserted into tobacco ( Nicotiana tabacum) using disarmed Agrobacterium tumefaciens (LBA4404) containing a binary expression vector. PLRV CP gene transcript was detected in transgenic plants but its abundance differed between transformed lines. CP was not detected in virus-free transgenic plants. The segregation of kanamycin resistance in S seedling progenies (obtained by selfing transformed plants) indicated that multiple (up to five) integration events involving vector T-DNA had occurred in most transformants. However, the amount of detectable CP transcript was not related to the neomycin phosphotransferase II gene copy number. Multiplication of PLRV in mature transgenic plants was diminished by up to 6-fold; the greatest diminution was in those transformed lines in which most CP gene transcript was detected. However, S progeny seedlings of transgenic plants were no more resistant to infection, following inoculation with viruliferous aphids, than seedlings of non-transformed control plants. [ABSTRACT FROM AUTHOR]

Questions on this topic that concern the clinician are addressed: whether it is inherited and, if so, whether Mendelian; what the segregation ratios will be; whether it is heterogeneous; how its high frequency can be accounted for; and what preventive measures are availabel. In several cases the question has to be reworded in order to make it sufficiently precise for it to be used in practice without misleading the patient. Framed in this fashion applicable answers are relatively easily available although many genetic puzzles remain. To date, no antenatal diagnosis is available. [ABSTRACT FROM AUTHOR]