scholarly journals Molecular Characterization of Two Types of Resistance in Sunflower to Plasmopara halstedii, the Causal Agent of Downy Mildew

2011 ◽  
Vol 101 (8) ◽  
pp. 970-979 ◽  
Author(s):  
Osman Radwan ◽  
Mohamed Fouad Bouzidi ◽  
Said Mouzeyar
Keyword(s):  
Downy Mildew ◽  
Interleukin 1 ◽  
Coiled Coil ◽  
Hypersensitive Reaction ◽  
Type I ◽  
Basal Region ◽  
Type Ii ◽  
Plasmopara Halstedii ◽  
Type I Resistance ◽  
Type Ii Resistance

Depending on host–pathotype combination, two types of sunflower–Plasmopara halstedii incompatibility reactions have previously been identified. Type I resistance can restrict the growth of the pathogen in the basal region of the hypocotyls, whereas type II cannot, thus allowing the pathogen to reach the cotyledons. In type II resistance, a large portion of the hypocotyls is invaded by the pathogen and, subsequently, a hypersensitive reaction (HR) is activated over a long portion of the hypocotyls. Thus, the HR in type II resistance coincides with a higher induction of hsr203j sunflower homologue in comparison with type I resistance, where the HR is activated only in the basal part of hypocotyls. Although the pathogen was not detected in cotyledons of type I resistant plants, semiquantitative polymerase chain reaction confirmed the early abundant growth of the pathogen in cotyledons of susceptible plants by 6 days postinfection (dpi). This was in contrast to scarce growth of the pathogen in cotyledons of type II-resistant plants at a later time point (12 dpi). This suggests that pathogen growth differs according to the host–pathogen combination. To get more information about sunflower downy mildew resistance genes, the full-length cDNAs of RGC151 and RGC203, which segregated with the PlARG gene (resistance type I) and Pl14 gene (resistance type II), were cloned and sequenced. Sequence analyses revealed that RGC151 belongs to the Toll/interleukin-1 receptor (TIR) nucleotide-binding site leucine-rich repeat (NBS-LRR) class whereas RGC203 belongs to class coiled-coil (CC)-NBS-LRR. This study suggests that type II resistance may be controlled by CC-NBS-LRR gene transcripts which are enhanced upon infection by P. halstedii, rather than by the TIR-NBS-LRR genes that might control type I resistance.

Genetic characterization of QTL associated with resistance to Fusarium head blight in a doubled-haploid spring wheat population

Genome ◽  
2005 ◽  
Vol 48 (2) ◽  
pp. 187-196 ◽  
Author(s):  
Zhuping Yang ◽  
Jeannie Gilbert ◽  
George Fedak ◽  
Daryl J Somers
Keyword(s):  
Spring Wheat ◽  
Resistance Genes ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Kernel Infection ◽  
Wheat Population ◽  
Fhb Resistance ◽  
Type I Resistance ◽  
Type Ii Resistance

Fusarium head blight (FHB) is one of the most important fungal wheat diseases worldwide. Understanding the genetics of FHB resistance is the key to facilitating the introgression of different FHB resistance genes into adapted wheat. The objectives of the present study were to detect and map quantitative trait loci (QTL) associated with FHB resistance genes and characterize the genetic components of the QTL in a doubled-haploid (DH) spring wheat population using both single-locus and two-locus analysis. A mapping population, consisting of 174 DH lines from the cross between DH181 (resistant) and AC Foremost (susceptible), was evaluated for type I resistance to initial infection during a 2-year period in spray-inoculated field trials, for Type II resistance to fungal spread within the spike in 3 greenhouse experiments using single-floret inoculation, and for resistance to kernel infection in a 2001 field trial. One-locus QTL analysis revealed 7 QTL for type I resistance on chromosome arms 2DS, 3AS, 3BS, 3BC (centromeric), 4DL, 5AS, and 6BS, 4 QTL for type II resistance on chromosomes 2DS, 3BS, 6BS, and 7BL, and 6 QTL for resistance to kernel infection on chromosomes 1DL, 2DS, 3BS, 3BC, 4DL, and 6BS. Two-locus QTL analysis detected 8 QTL with main effects and 4 additive by additive epistatic interactions for FHB resistance and identified novel FHB resistance genes for the first time on chromosomes 1DL, 4AL, and 4DL. Neither significant QTL by environment interactions nor epistatic QTL by environment interactions were found for either type I or type II resistance. The additive effects of QTL explained most of the phenotypic variance for FHB resistance. Marker-assisted selection for the favored alleles at multiple genomic regions appears to be a promising tool to accelerate the introgression and pyramiding of different FHB resistance genes into adapted wheat genetic backgrounds.Key words: Triticum aestivum, Fusarium graminearum, microsatellite, additive effect, additive by additive epistatic effect.

scholarly journals Mapping Resistance to Argentinean Fusarium (Graminearum) Head Blight Isolates in Wheat

2021 ◽  
Vol 22 (24) ◽  
pp. 13653
Author(s):  
Carolina Sgarbi ◽  
Ismael Malbrán ◽  
Luciana Saldúa ◽  
Gladys Albina Lori ◽  
Ulrike Lohwasser ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Wheat Yield ◽  
Kernel Weight ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Yield And Quality ◽  
Type I Resistance ◽  
Additive Qtls ◽  
Type Ii Resistance

Fusarium head blight (FHB) of wheat, caused by Fusarium graminearum (Schwabe), is a destructive disease worldwide, reducing wheat yield and quality. To accelerate the improvement of scab tolerance in wheat, we assessed the International Triticeae Mapping Initiative mapping population (ITMI/MP) for Type I and II resistance against a wide population of Argentinean isolates of F. graminearum. We discovered a total of 27 additive QTLs on ten different (2A, 2D, 3B, 3D, 4B, 4D, 5A, 5B, 5D and 6D) wheat chromosomes for Type I and Type II resistances explaining a maximum of 15.99% variation. Another four and two QTLs for thousand kernel weight in control and for Type II resistance, respectively, involved five different chromosomes (1B, 2D, 6A, 6D and 7D). Furthermore, three, three and five QTLs for kernel weight per spike in control, for Type I resistance and for Type II resistance, correspondingly, involved ten chromosomes (2A, 2D, 3B, 4A, 5A, 5B, 6B, 7A, 7B, 7D). We were also able to detect five and two epistasis pairs of QTLs for Type I and Type II resistance, respectively, in addition to additive QTLs that evidenced that FHB resistance in wheat is controlled by a complex network of additive and epistasis QTLs.

scholarly journals Quantitative Trait Loci for Fusarium Head Blight Resistance in a Recombinant Inbred Population of Wangshuibai/Wheaton

2008 ◽  
Vol 98 (1) ◽  
pp. 87-94 ◽  
Author(s):  
J.-B. Yu ◽  
G.-H. Bai ◽  
W.-C. Zhou ◽  
Y.-H. Dong ◽  
F. L. Kolb
Keyword(s):  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Recombinant Inbred ◽  
Type I ◽  
Type Ii ◽  
Head Blight ◽  
Type Iii ◽  
Fhb Resistance ◽  
Type I Resistance ◽  
Type Ii Resistance

Use of diverse sources of Fusarium head blight (FHB)-resistant germplasm in breeding may significantly improve wheat resistance to FHB. Wangshuibai is an FHB-resistant Chinese landrace unrelated to cv. Sumai 3, the most commonly used FHB-resistant source. In all, 139 F6 recombinant inbred lines were developed from a cross between Wangshuibai and an FHB-susceptible cultivar, Wheaton, to map quantitative trait loci (QTL) for wheat resistance to initial infection (type I resistance), spread of FHB symptoms within a spike (type II resistance), and deoxynivalenol (DON) accumulation (type III resistance) in infected grain. The experiments were conducted in a greenhouse at Manhattan, KS from 2003 to 2005. More than 1,300 simple-sequence repeat and amplified fragment length polymorphism markers were analyzed in this population. Five QTL for type I resistance were detected on chromosomes 3AS, 3BS, 4B, 5AS, and 5DL after spray inoculation; seven QTL for type II resistance were identified on chromosomes 1A, 3BS, 3DL, 5AS, 5DL, and 7AL after point inoculation; and seven QTL for type III resistance were detected on chromosomes 1A, 1BL, 3BS, 5AS, 5DL, and 7AL with the data from both inoculation methods. These QTL jointly explained up to 31.7, 64, and 52.8% of the phenotypic variation for the three types of FHB resistance, respectively. The narrow-sense heritabilities were low for type I resistance (0.37 to 0.41) but moderately high for type II resistance (0.45 to 0.61) and type III resistance (0.44 to 0.67). The QTL on the distal end of 3BS, 5AS, and 5DL contributed to all three types of resistance. Two QTL, on 7AL and 1A, as well as one QTL near the centromere of 3BS (3BSc), showed effects on both type II and type III resistance. Selection for type II resistance may simultaneously improve type I and type III resistance as well. The QTL for FHB resistance identified in Wangshuibai have potential to be used to pyramid FHB-resistance QTL from different sources.

scholarly journals Independent binding of interleukin-1 alpha and interleukin-1 beta to type I and type II interleukin-1 receptors.

1993 ◽  
Vol 268 (4) ◽  
pp. 2513-2524
Author(s):  
J. Slack ◽  
C.J. McMahan ◽  
S. Waugh ◽  
K. Schooley ◽  
M.K. Spriggs ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Type I ◽  
Type Ii ◽  
Interleukin 1 Beta

scholarly journals A chimeric type II/type I interleukin-1 receptor can mediate interleukin-1 induction of gene expression in T cells

1993 ◽  
Vol 268 (14) ◽  
pp. 10490-10494
Author(s):  
A. Heguy ◽  
C.T. Baldari ◽  
S. Censini ◽  
P. Ghiara ◽  
J.L. Telford
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Interleukin 1 ◽  
Type I ◽  
Type Ii

Interleukin-1 alpha stimulates dopamine release by activating type II protein kinase A in PC-12 cells

1995 ◽  
Vol 269 (6) ◽  
pp. E1083-E1088
Author(s):  
A. Joseph ◽  
A. Kumar ◽  
N. A. O'Connell ◽  
R. K. Agarwal ◽  
A. R. Gwosdow
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Dopamine Release ◽  
Interleukin 1 ◽  
Intracellular Camp ◽  
Type I ◽  
Camp Accumulation ◽  
Type Ii ◽  
Pc 12 Cells ◽  
Kinase A

A recent study from this laboratory [A. R. Gwosdow, N. A. O'Connell, and A. B. Abou-Samra. Am. J. Physiol. 263 (Endocrinol. Metab. 26): E461-E466, 1992] showed that the inflammatory mediator interleukin-1 alpha (IL-1 alpha) stimulates catecholamine release from primary cultures of rat adrenal cells. The present studies were conducted to determine whether 1) IL-1 alpha stimulates catecholamine/dopamine release from the adrenal medullary cell line PC-12 and 2) the adenosine 3',5'-cyclic monophosphate (cAMP)-protein kinase A (PKA) pathway is involved in IL-1 alpha-induced dopamine release from PC-12 cells. The results indicate that IL-1 alpha significantly (P < 0.05) elevated dopamine release after a 24-h incubation period. IL-1 alpha did not stimulate cAMP accumulation at any time period between 5 min and 2 h. In contrast, forskolin-treated cells elevated (P < 0.05) intracellular cAMP levels and increased dopamine release. Because IL-1 alpha did not affect cAMP accumulation, the effect of IL-1 alpha on PKA activity was investigated. IL-1 alpha increased (P < 0.05) PKA activity at 15 and 30 min and returned to control levels by 1 h. Forskolin also increased (P < 0.05) PKA activity. The type of PKA activated (P < 0.05) by IL-1 alpha was type II PKA. In contrast, forskolin activated (P < 0.05) type I and type II PKA. Inhibition of PKA with the PKA inhibitor H-8 blocked PKA activity and dopamine secretion by both IL-1 alpha and forskolin in PC-12 cells. These observations demonstrate that 1) IL-1 alpha stimulated dopamine release from PC-12 cells by activating PKA, 2) the mechanism of IL-1 alpha activation of PKA does not involve detectable increases in intracellular cAMP accumulation, and 3) IL-1 alpha activates type II PKA, which is used by IL-1 alpha to stimulate dopamine secretion from PC-12 cells.

Human aortic endothelial cells express the type I but not the type II receptor for interleukin-1 (IL-1)

1992 ◽  
Vol 153 (3) ◽  
pp. 583-588 ◽  
Author(s):  
Ann L. Akeson ◽  
Laura B. Mosher ◽  
Connie W. Woods ◽  
Kendra K. Schroeder ◽  
Terry L. Bowlin
Keyword(s):  
Endothelial Cells ◽  
Interleukin 1 ◽  
Type I ◽  
Type Ii ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Type I and Type II Interleukin-1 Receptor Expression in Rat, Mouse, and Human Testes1

1997 ◽  
Vol 56 (6) ◽  
pp. 1513-1526 ◽  
Author(s):  
Edith Gomez ◽  
Gérard Morel ◽  
Annie Cavalier ◽  
Marie-Odile Liénard ◽  
France Haour ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Receptor Expression ◽  
Type I ◽  
Type Ii
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