Expansive Phenotypic Landscape of Botrytis cinerea Shows Differential Contribution of Genetic Diversity and Plasticity

Abstract

*The e-Xtra logo stands for "electronic extra" and indicates that seven supplementary figures and five supplementary tables are published online.

Plastic Transcriptomes Stabilize Immunity to Pathogen Diversity: The Jasmonic Acid and Salicylic Acid Networks within the Arabidopsis/Botrytis Pathosystem

“…Thus, it does not appear that there is any singular gene or subset of genes that are highly correlated with resistance and lesion area. This supports the perspective that host resistance to B. cinerea is extremely polygenic (Corwin et al, 2016a). Interestingly, three of the top 10 highest positively correlated genes encode a chitinase, a chitininducible gene (AT5G25260), and a PAMP-inducible kinase FRK1 (Passarinho et al, 2001;Millet et al, 2010;Yeh et al, 2016;Nie et al, 2017).…”

“…Previous studies using one or a few B. cinerea isolates to focus on genetic difference in the Arabidopsis host have shown a negative correlation between camalexin content and lesion area across host genotypes (Ferrari et al, 2003;Denby et al, 2004;Corwin et al, 2016aCorwin et al, , 2016b. This larger population of B. cinerea isolates allows us to test how genetic diversity in the pathogen influences the effectiveness of plant molecular defenses, specifically camalexin.…”

“…To test how genetic variation within the species B. cinerea differentially probes the major plant defense pathways, we infected a collection of 96 diverse B. cinerea isolates onto the Col-0 accession of Arabidopsis (Supplemental Data Set 1) (Atwell et al, 2015;Corwin et al, 2016a). This collection of natural isolates was obtained mainly from California with a sampling of available international germplasm.…”

“…This collection of natural isolates was obtained mainly from California with a sampling of available international germplasm. They represent a wide range of genomic, phenotypic, and virulence variation (Rowe and Kliebenstein, 2007;Atwell et al, 2015;Corwin et al, 2016a). In conjunction with wild-type Col-0, we also included the immuno-compromised, single-gene knockout mutants coi1-1 and npr1-1, which abolish or diminish the major defense processing of the JA and SA pathways respectively (Xie et al, 1998;Xu et al, 2002;Thines et al, 2007;Chini et al, 2009;Sheard et al, 2010;Yan and Dong, 2014).…”

“…B. cinerea has elevated natural genetic variation that results in multiple major-effect polymorphisms in known virulence mechanisms, including the production of phytotoxic metabolites (Colmenares et al, 2002;Dalmais et al, 2011), enzymes that detoxify plant defense metabolites (Ferrari et al, 2003;Pedras et al, 2005Pedras et al, , 2007Pedras et al, , 2008Pedras et al, , 2009Pedras et al, , 2011Stefanato et al, 2009;Rowe et al, 2010), and the ability to degrade plant cell walls (Rowe and Kliebenstein, 2007;Schumacher et al, 2012Schumacher et al, , 2015Kumari et al, 2014). Because wild B. cinerea isolates have recombination and random mating, a population of isolates is a random intermixed sample of the diverse virulence mechanisms (Rowe and Kliebenstein, 2007;Kretschmer et al, 2009;Rowe et al, 2010;Kumari et al, 2014;Atwell et al, 2015;Corwin et al, 2016aCorwin et al, , 2016bZhang et al, 2016). This allows us to use a population of isolates to challenge a plant's innate immune system with a diverse array of natural inputs from a single pathogen species and assess the flexibility of the signaling network (Finkers et al, 2007a(Finkers et al, , 2007bRowe and Kliebenstein, 2008;Davis et al, 2009;Corwin et al, 2016b;Zhang et al, 2016).…”