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QTL analysis for sugar‐regulated leaf senescence supports flowering‐dependent and ‐independent senescence pathways
Author(s) -
Wingler Astrid,
Purdy Sarah Jane,
Edwards SallyAnne,
Chardon Fabien,
MasclauxDaubresse Céline
Publication year - 2010
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.2009.03072.x
Subject(s) - senescence , quantitative trait locus , biology , vernalization , population , arabidopsis , genetics , botany , gene , mutant , demography , sociology
Summary• The aim of this work was to determine the genetic basis of sugar‐regulated senescence and to explore the relationship with other traits, including flowering and nitrogen‐use efficiency. • Quantitative trait loci (QTLs) for senescence were mapped in the Arabidopsis Bay‐0 × Shahdara recombinant‐inbred line (RIL) population after growth on glucose‐containing medium, which accelerates senescence. The extent of whole‐rosette senescence was determined by imaging the maximum quantum yield of photosystem II ( F v / F m ). • A major QTL on the top of chromosome 4 colocalized with FRI , a major determinant of flowering. This QTL interacted epistatically with a QTL on chromosome 5, where the floral repressor FLC localizes. Vernalization accelerated senescence in late‐flowering lines with functional FRI and FLC alleles. Comparison with previous results using the Bay‐0 × Shahdara population showed that rapid rosette senescence on glucose‐containing medium was correlated with early flowering and high sugar content in compost‐grown plants. In addition, correlation was found between the expression of flowering and senescence‐associated genes in Arabidopsis accessions. However, an additional QTL on chromosome 3 was not linked to flowering, but to nitrogen‐use efficiency. • The results show that whole‐rosette senescence is genetically linked to the vernalization‐dependent control of flowering, but is also controlled by flowering‐independent pathways.

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