Celine Caseys

Celine Caseys

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Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 February 2016 in Evolutionary Applications
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MTMarco Todesco
Marco Todesco
MPMariana A. Pascual
Mariana A. Pascual
GOGregory L. Owens
Gregory L. Owens
KOKate Ostevik
Kate Ostevik
BMBrook T. Moyers
Brook T. Moyers
LRLoren H. Rieseberg
Loren H. Rieseberg
Hybridization may drive rare taxa to extinction through genetic swamping, where the rare form is replaced by hybrids, or by demographic swamping, where population growth rates are reduced due to the wasteful production of maladaptive hybrids. Conversely, hybridization may rescue the viability of small, inbred populations. Understanding the factors that contribute to destructive versus constructive outcomes of hybridization is key to managing conservation concerns. Here, we survey the literature for studies of hybridization and extinction to identify the ecological, evolutionary, and genetic factors that critically affect extinction risk through hybridization. We find that while extinction risk is highly situation dependent, genetic swamping is much more frequent than demographic swamping. In addition, human involvement is associated with increased risk and high reproductive isolation with reduced risk. Although climate change is predicted to increase the risk of hybridization‐induced extinction, we find little empirical support for this prediction. Similarly, theoretical and experimental studies imply that genetic rescue through hybridization may be equally or more probable than demographic swamping, but our literature survey failed to support this claim. We conclude that halting the introduction of hybridization‐prone exotics and restoring mature and diverse habitats that are resistant to hybrid establishment should be management priorities.

9 January 2015 in Molecular Ecology
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Journal Article
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DBDan Bock
Dan Bock
CCCeline Caseys
Celine Caseys
RCRoger D. Cousens
Roger D. Cousens
MHMin A. Hahn
Min A. Hahn
SHSylvia M. Heredia
Sylvia M. Heredia
LRLoren H. Rieseberg
Loren H. Rieseberg

12 September 2012 in Molecular Ecology
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Journal Article
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KSKai N. Stölting
Kai N. Stölting
RNRick Nipper
Rick Nipper
DLDorothea Lindtke
Dorothea Lindtke
CCCeline Caseys
Celine Caseys
SWStephan Waeber
Stephan Waeber
CLChristian Lexer
Christian Lexer

7 May 2018 in Nature Ecology & Evolution
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DBDan Bock
Dan Bock
MKMichael Kantar
Michael Kantar
CCCeline Caseys
Celine Caseys
RMRemi Matthey-Doret
Remi Matthey-Doret
LRLoren H. Rieseberg
Loren H. Rieseberg

1 December 2023 in Molecular Plant Pathology
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Journal Article
Open access
RSRitu Singh
Ritu Singh
CCCeline Caseys
Celine Caseys
DKDaniel J. Kliebenstein
Daniel J. Kliebenstein
Botrytis cinerea Pers. Fr. (teleomorph: Botryotinia fuckeliana ) is a necrotrophic fungal pathogen that attacks a wide range of plants. This updated pathogen profile explores the extensive genetic diversity of B. cinerea , highlights the progress in genome sequencing, and provides current knowledge of genetic and molecular mechanisms employed by the fungus to attack its hosts. In addition, we also discuss recent innovative strategies to combat B. cinerea . Taxonomy: Kingdom: Fungi, phylum: Ascomycota, subphylum: Pezizomycotina, class: Leotiomycetes, order: Helotiales, family: Sclerotiniaceae, genus: Botrytis , species: cinerea . Host range: B. cinerea infects almost all of the plant groups (angiosperms, gymnosperms, pteridophytes, and bryophytes). To date, 1606 plant species have been identified as hosts of B. cinerea . Genetic diversity: This polyphagous necrotroph has extensive genetic diversity at all population levels shaped by climate, geography, and plant host variation. Pathogenicity: Genetic architecture of virulence and host specificity is polygenic using multiple weapons to target hosts, including secretory proteins, complex signal transduction pathways, metabolites, and mobile small RNA. Disease control strategies: Efforts to control B. cinerea , being a high‐diversity generalist pathogen, are complicated. However, integrated disease management strategies that combine cultural practices, chemical and biological controls, and the use of appropriate crop varieties will lessen yield losses. Recently, studies conducted worldwide have explored the potential of small RNA as an efficient and environmentally friendly approach for combating grey mould. However, additional research is necessary, especially on risk assessment and regulatory frameworks, to fully harness the potential of this technology.

18 May 2021 in G3: Genes, Genomes, Genetics
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Journal Article
Open access
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CCCeline Caseys
Celine Caseys
GSGongjun Shi
Gongjun Shi
NSNicole Soltis
Nicole Soltis
RGRaoni Gwinner
Raoni Gwinner
JCJason Corwin
Jason Corwin
DKDaniel J Kliebenstein
Daniel J Kliebenstein
Botrytis cinerea is a fungal pathogen that causes necrotic disease on more than a thousand known hosts widely spread across the plant kingdom. How B. cinerea interacts with such extensive host diversity remains largely unknown. To address this question, we generated an infectivity matrix of 98 strains of B. cinerea on 90 genotypes representing eight host plants. This experimental infectivity matrix revealed that the disease outcome is largely explained by variations in either the host resistance or pathogen virulence. However, the specific interactions between host and pathogen account for 16% of the disease outcome. Furthermore, the disease outcomes cluster among genotypes of a species but are independent of the relatedness between hosts. When analyzing the host specificity and virulence of B. cinerea, generalist strains are predominant. In this fungal necrotroph, specialization may happen by a loss in virulence on most hosts rather than an increase of virulence on a specific host. To uncover the genetic architecture of Botrytis host specificity and virulence, a genome-wide association study (GWAS) was performed and revealed up to 1492 genes of interest. The genetic architecture of these traits is widespread across the B. cinerea genome. The complexity of the disease outcome might be explained by hundreds of functionally diverse genes putatively involved in adjusting the infection to diverse hosts.