CIRCADIAN CLOCK-ASSOCIATED1 Controls Resistance to Aphids by Altering Indole Glucosinolate Production

Simple item page
dc.citation.firstpage1344en_US
dc.citation.issueNumber3en_US
dc.citation.journalTitlePlant Physiologyen_US
dc.citation.lastpage1359en_US
dc.citation.volumeNumber181en_US
dc.contributor.authorLei, Jiaxinen_US
dc.contributor.authorJayaprakasha, Guddadarangavvanahally K.en_US
dc.contributor.authorSingh, Jashbiren_US
dc.contributor.authorUckoo, Rammohanen_US
dc.contributor.authorBorrego, Eli J.en_US
dc.contributor.authorFinlayson, Scotten_US
dc.contributor.authorKolomiets, Mikeen_US
dc.contributor.authorPatil, Bhimanagouda S.en_US
dc.contributor.authorBraam, Janeten_US
dc.contributor.authorZhu-Salzman, Keyanen_US
dc.date.accessioned2021-10-06T14:15:52Zen_US
dc.date.available2021-10-06T14:15:52Zen_US
dc.date.issued2019en_US
dc.description.abstractCIRCADIAN CLOCK-ASSOCIATED1 (CCA1), a well-known central circadian clock regulator, coordinates plant responses to environmental challenges. Its daily rhythmic expression in Arabidopsis (Arabidopsis thaliana) confers host resistance to the caterpillar Trichoplusia ni. However, it is unclear whether CCA1 plays a role in defense against phloem sap-feeding aphids. In this study, we showed that green peach aphid (Myzus persicae) displayed an intrinsic circadian feeding rhythm. Under constant light, wild-type Columbia-0 (Col-0) Arabidopsis plants coentrained with aphids in the same light/dark cycles exhibited greater antixenotic activity than plants preentrained in the opposite cycle from the aphids. Consistently, circadian mutants cca1-1, cca1-11, lhy-21, ztl-1, ztl-4, and lux-2 suffered more severe damage than Col-0 plants when infested by aphids, suggesting that the Arabidopsis circadian clock plays a defensive role. However, the arrhythmic CCA1 overexpression line (CCA1-OX) displayed strong antixenotic and antibiotic activities despite its loss of circadian regulation. Aphids feeding on CCA1-OX plants exhibited lower reproduction and smaller body size and weight than those on Col-0. Apparently, CCA1 regulates both clock-dependent and -independent defense responses. Systematic investigation based on bioinformatics analyses indicated that resistance to aphids in CCA1-OX plants was due primarily to heightened basal indole glucosinolate levels. Interestingly, aphid feeding induced alternatively spliced intron-retaining CCA1a/b transcripts, which are normally expressed at low levels, whereas expression of the major fully spliced CCA1 transcript remained largely unchanged. We hypothesize that posttranscriptional modulation of CCA1 expression upon aphid infestation maximizes the potential of circadian-mediated defense and stress tolerance while ensuring normal plant development.en_US
dc.identifier.citationLei, Jiaxin, Jayaprakasha, Guddadarangavvanahally K., Singh, Jashbir, et al.. "CIRCADIAN CLOCK-ASSOCIATED1 Controls Resistance to Aphids by Altering Indole Glucosinolate Production." <i>Plant Physiology,</i> 181, no. 3 (2019) Oxford University Press: 1344-1359. https://doi.org/10.1104/pp.19.00676.en_US
dc.identifier.digitalplphys_v181_3_1344en_US
dc.identifier.doihttps://doi.org/10.1104/pp.19.00676en_US
dc.identifier.urihttps://hdl.handle.net/1911/111488en_US
dc.language.isoengen_US
dc.publisherOxford University Pressen_US
dc.rightsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.titleCIRCADIAN CLOCK-ASSOCIATED1 Controls Resistance to Aphids by Altering Indole Glucosinolate Productionen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
plphys_v181_3_1344.pdf
Size:
1.55 MB
Format:
Adobe Portable Document Format
Download
Collections
Faculty Publications
Biochemistry and Cell Biology Publications