Genetic variation and segregation of DNA polymorphisms in Botrytis cinerea

1993 ◽  
Vol 97 (10) ◽  
pp. 1193-1200 ◽  
Author(s):  
C.J.B. Van Der Vlugt-Bergmans ◽  
B.F. Brandwagt ◽  
J.W. Vant't Klooster ◽  
C.A.M. Wagemakers ◽  
J.A.L. Van Kan
2020 ◽  
Vol 38 (3) ◽  
pp. 187-199
Author(s):  
Loubna Dibeh ◽  
◽  
Omar Hammoudi ◽  
Ahmad Mouhanna ◽  
◽  
...  

2007 ◽  
Vol 20 (9) ◽  
pp. 1126-1137 ◽  
Author(s):  
Heather C. Rowe ◽  
Daniel J. Kliebenstein

Botrytis cinerea, or gray mold, is a necrotrophic fungal pathogen of hundreds of plant species. The genetic diversity of B. cinerea may contribute to its broad host range; however, the level and structure of genetic variation at pathogenesis-associated loci has not been described. B. cinerea possesses six distinct cell-wall-degrading polygalacturonases (PGs), enzymes of demonstrated importance to pathogenesis and interaction with host plant defenses. Sequencing a collection of 34 B. cinerea isolates at three PG-encoding loci, BcPG1, BcPG2, and BcPG3, revealed limited evidence of host-mediated genetic subdivision within loci, yet suggested differences in the action of evolutionary forces among loci. BcPG1 and BcPG2 are highly polymorphic, particularly when compared with previously published data from nonpathogenicity loci, whereas BcPG3 is relatively conserved. Sequence variation at BcPG1 and BcPG2 did not appear to be associated with virulence on Arabidopsis leaves; however, BcPG2 variation showed a statistically significant association with growth rate on pectin. Rather than providing evidence for host-mediated genetic subdivision at individual PG loci, our data support specialization among PGs and the potential diversification of PGs interacting directly with host defenses.


Genetics ◽  
1993 ◽  
Vol 135 (4) ◽  
pp. 1187-1196
Author(s):  
Y P Hong ◽  
V D Hipkins ◽  
S H Strauss

Abstract The amount, distribution and mutational nature of chloroplast DNA polymorphisms were studied via analysis of restriction fragment length polymorphisms in three closely related species of conifers, the California closed-cone pines-knobcone pine: Pinus attenuata Lemm.; bishop pine: Pinus muricata D. Don; and Monterey pine: Pinus radiata D. Don. Genomic DNA from 384 trees representing 19 populations were digested with 9-20 restriction enzymes and probed with cloned cpDNA fragments from Douglas-fir [Pseudotsuga menziesii (Mirb.) Franco] that comprise 82% chloroplast genome. Up to 313 restriction sites were surveyed, and 25 of these were observed to be polymorphic among or within species. Differences among species accounted for the majority of genetic (haplotypic) diversity observed [Gst = 84(+/- 13)%]; nucleotide diversity among species was estimated to be 0.3(+/- 0.1)%. Knobcone pine and Monterey pine displayed almost no genetic variation within or among populations. Bishop pine also showed little variability within populations, but did display strong population differences [Gst = 87(+/- 8)%] that were a result of three distinct geographic groups. Mean nucleotide diversity within populations was 0.003(+/- 0.002)%; intrapopulation polymorphisms were found in only five populations. This pattern of genetic variation contrasts strongly with findings from study of nuclear genes (allozymes) in the group, where most genetic diversity resides within populations rather than among populations or species. Regions of the genome subject to frequent length mutations were identified; estimates of subdivision based on length variant frequencies in one region differed strikingly from those based on site mutations or allozymes. Two trees were identified with a major chloroplast DNA inversion that closely resembled one documented between Pinus and Pseudotsuga.


2010 ◽  
Vol 9 (46) ◽  
pp. 7961-7967 ◽  
Author(s):  
P Suresh ◽  
e ◽  
Sharma Mamta ◽  
Krishna Kishore G ◽  
Shivram L ◽  
...  

2013 ◽  
Vol 136 (2) ◽  
pp. 407-417 ◽  
Author(s):  
Bernard A. Wessels ◽  
Sandra C. Lamprecht ◽  
Celeste C. Linde ◽  
Paul H. Fourie ◽  
Lizel Mostert

Author(s):  
Stefan Petrasch ◽  
Saskia D Mesquida-Pesci ◽  
Dominique D A Pincot ◽  
Mitchell J Feldmann ◽  
Cindy M López ◽  
...  

Abstract Gray mold, a disease of strawberry (Fragaria × ananassa) caused by the ubiquitous necrotroph Botrytis cinerea, renders fruit unmarketable and causes economic losses in the postharvest supply chain. To explore the feasibility of selecting for increased resistance to gray mold, we undertook genetic and genomic prediction studies in strawberry populations segregating for fruit quality and shelf life traits hypothesized to pleiotropically affect susceptibility. As predicted, resistance to gray mold was heritable but quantitative and genetically complex. While every individual was susceptible, the speed of symptom progression and severity differed. Narrow-sense heritability ranged from 0.38 to 0.71 for lesion diameter (LD) and 0.39 to 0.44 for speed of emergence of external mycelium (EM). Even though significant additive genetic variation was observed for LD and EM, the phenotypic ranges were comparatively narrow and genome-wide analyses did not identify any large-effect loci. Genomic selection (GS) accuracy ranged from 0.28 to 0.59 for LD and 0.37 to 0.47 for EM. Additive genetic correlations between fruit quality and gray mold resistance traits were consistent with prevailing hypotheses: LD decreased as titratable acidity increased, whereas EM increased as soluble solid content decreased and firmness increased. We concluded that phenotypic and GS could be effective for reducing LD and increasing EM, especially in long shelf life populations, but that a significant fraction of the genetic variation for resistance to gray mold was caused by the pleiotropic effects of fruit quality traits that differ among market and shelf life classes.


Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 915-929
Author(s):  
Z W Luo ◽  
Chung-I Wu ◽  
M J Kearsey

Abstract Dissecting quantitative genetic variation into genes at the molecular level has been recognized as the greatest challenge facing geneticists in the twenty-first century. Tremendous efforts in the last two decades were invested to map a wide spectrum of quantitative genetic variation in nearly all important organisms onto their genome regions that may contain genes underlying the variation, but the candidate regions predicted so far are too coarse for accurate gene targeting. In this article, the recurrent selection and backcross (RSB) schemes were investigated theoretically and by simulation for their potential in mapping quantitative trait loci (QTL). In the RSB schemes, selection plays the role of maintaining the recipient genome in the vicinity of the QTL, which, at the same time, are rapidly narrowed down over multiple generations of backcrossing. With a high-density linkage map of DNA polymorphisms, the RSB approach has the potential of dissecting the complex genetic architecture of quantitative traits and enabling the underlying QTL to be mapped with the precision and resolution needed for their map-based cloning to be attempted. The factors affecting efficiency of the mapping method were investigated, suggesting guidelines under which experimental designs of the RSB schemes can be optimized. Comparison was made between the RSB schemes and the two popular QTL mapping methods, interval mapping and composite interval mapping, and showed that the scenario of genomic distribution of QTL that was unlocked by the RSB-based mapping method is qualitatively distinguished from those unlocked by the interval mapping-based methods.


2007 ◽  
Vol 6 (8) ◽  
pp. 1174-1181 ◽  
Author(s):  
Christian Joseph R. . ◽  
Heiko P. Parzies . ◽  
Thomas Miedaner .

2016 ◽  
Vol 29 (4) ◽  
pp. 287-298 ◽  
Author(s):  
Jason A. Corwin ◽  
Anushriya Subedy ◽  
Robert Eshbaugh ◽  
Daniel J. Kliebenstein

The modern evolutionary synthesis suggests that both environmental variation and genetic diversity are critical determinants of pathogen success. However, the relative contribution of these two sources of variation is not routinely measured. To estimate the relative contribution of plasticity and genetic diversity for virulence-associated phenotypes in a generalist plant pathogen, we grew a population of 15 isolates of Botrytis cinerea from throughout the world, under a variety of in vitro and in planta conditions. Under in planta conditions, phenotypic differences between the isolates were determined by the combination of genotypic variation within the pathogen and environmental variation. In contrast, phenotypic differences between the isolates under in vitro conditions were predominantly determined by genetic variation in the pathogen. Using a correlation network approach, we link the phenotypic variation under in vitro experimental conditions to phenotypic variation during plant infection. This study indicates that there is a high level of phenotypic variation within B. cinerea that is controlled by a mixture of genetic variation, environment, and genotype × environment. This argues that future experiments into the pathogenicity of B. cinerea must account for the genetic and environmental variation within the pathogen to better sample the potential phenotypic space of the pathogen.


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