PEDIATRICS ◽  
1979 ◽  
Vol 63 (6) ◽  
pp. 890-893
Author(s):  
Marvin E. Miller ◽  
David W. Smith

Two families are described in which there is possible monogenic inheritance of congenital cardiac defects within the spectrum of faulty conotruncal septation (CTS). Evidence for a genetic control of conotruncal septation arises from genetic and embryologic studies of similar defects in the Keeshond dog model, the excess of sibship pairs with conotruncal septation defects in sibship pairs with congenital heart disease, and previously reported pedigrees of families with multiple affected individuals with conotruncal septation defects. It is suggested that in the small number of cases of congenital cardiac defects in which there is a strong family history for CTS defects, a higher recurrence risk should be considered rather than the usual polygenic recurrence risk of 3% that is usually given in such situations.


2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 612-614
Author(s):  
N. Mironenko ◽  
O. Filatova ◽  
O. Afanasenko

Ascospore progeny of cross of Pyrenophora teres f. teres isolates was evaluated on virulence to three barley genotypes. Monogenic inheritance of virulence (26 a:17 v and 31 a:18 v) was shown to cultivar Harbin and accession c 21272 and supported by results of two fungal backcrosses. The existence of three unlinked avirulence genes to CI 4922 is suggested (37 a:7 v). The model of interaction between barley resistance genes and avirulence genes with postulated fungal genotypes is proposed.


Epilepsia ◽  
1999 ◽  
Vol 40 (s3) ◽  
pp. 4-8 ◽  
Author(s):  
Andreas Ziegler

2014 ◽  
Vol 134 (1) ◽  
pp. 105-110 ◽  
Author(s):  
Dharmendra Singh ◽  
Harsh Kumar Dikshit ◽  
Arun Kumar

2015 ◽  
Vol 62 (4) ◽  
pp. 980-981 ◽  
Author(s):  
Marcin Krawczyk ◽  
Caroline S. Stokes ◽  
Stefano Romeo ◽  
Frank Lammert

2012 ◽  
Vol 10 (1) ◽  
pp. 19-26
Author(s):  
Viktor E Tsyganov ◽  
Vera A Voroshilova ◽  
Sergey M Rozov ◽  
Aleksey U Borisov ◽  
Igor A Tikhonovich

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


Author(s):  
Jeferson Araújo Silva ◽  
Antonio Félix da Costa ◽  
Ana Maria Benko-Iseppon ◽  
Lílian Margarete Paes Guimarães ◽  
Diego Arruda Huggins de Sá Leitão ◽  
...  

Abstract: The objective of this work was to evaluate the inheritance of resistance to Cowpea aphid-borne mosaic virus (CABMV) in cowpea (Vigna unguiculata). The study was performed between parental genotypes IT85F-2687 (resistant) and 'BR-14 Mulato' (susceptible), generating F1, F2, and F7 populations and backcrosses with both parental genotypes. CABMV was inoculated on plants from all generations, which were then evaluated through visual inspection and description of characteristic symptoms. A chi-square test was performed after the phenotypic classification of all plants. A segregation proportion of 1:3 (resistant:susceptible) in population F2 and of 1:1 in population F7 was accepted, showing a recessive monogenic inheritance.


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