TheArabidopsis COMATOSElocus regulates germination potential

Abstract

Mutation of the COMATOSE locus in Arabidopsis results in a marked reduction in germination potential. Whilst the morphology of comatose (cts) embryos is not altered, physiological analysis reveals that mature cts seeds do not respond to gibberellin. Prolonged chilling of imbibed seeds only partially restores germination potential, and seeds do not after ripen. Genetic analysis shows that the cts phenotype is expressed in the embryo and phenotypic differences between wild-type and mutant plants were not observed during other stages of plant growth and development. Therefore cts represents a new class of mutant, with a specific lesion that results in severely impaired germination potential. Genetic interactions were analysed between cts and loci that regulate embryo maturation, and abscisic acid biosynthesis and perception. Results from these studies showed that the cts mutant phenotype required the wild-type action of these loci, and suggested that CTS exerts a repressive function on these loci. A model is presented postulating that CTS promotes increased germination potential, and represses embryo dormancy. These functions of CTS may result in the removal of embryo dormancy as a prerequisite to germination.

Control of germination and lipid mobilization by COMATOSE, the Arabidopsis homologue of human ALDP

“…The CTS gene was identified using a combination of positional cloning and insertional mutagenesis. Previously, the cts‐1 mutation had been mapped to the distal arm of chromosome IV, close to the marker DHS1 (Russell et al ., 2000). Southern analysis of chromosomal organization in this region revealed a polymorphism associated with cts‐1 within the predicted gene AT4G39850 (data not shown).…”

“…The COMATOSE ( CTS ) locus was identified genetically as having a very strong effect on the enhancement of germination (Russell et al ., 2000). cts mutant seeds do not germinate, and exhibit a ‘forever dormant’ phenotype (Russell et al ., 2000).…”

“…The COMATOSE ( CTS ) locus was identified genetically as having a very strong effect on the enhancement of germination (Russell et al ., 2000). cts mutant seeds do not germinate, and exhibit a ‘forever dormant’ phenotype (Russell et al ., 2000). This strong phenotype implicated CTS as a target for loci that repress germination, and suggests CTS is a major control point between dormancy and germination.…”

12-oxo-Phytodienoic Acid: A Fuse and/or Switch of Plant Growth and Defense Responses?

“…An earlier study of COMATOSE, a peroxisomal ATP-binding cassette transporter, and its mutant plants (cts) disrupted the transport of OPDA into the peroxisome, where JA biosynthesis occurs, illuminated a critical activity of OPDA signaling in coordinating seed germination and dormancy (Russell et al, 2000). The mutant cts seeds exhibited increased accumulation level of OPDA and low germination rates (Russell et al, 2000;Dave et al, 2011), while exogenous OPDA applications stimulated the repression of the germination of WT seeds (Dave et al, 2011).…”

“…An earlier study of COMATOSE, a peroxisomal ATP-binding cassette transporter, and its mutant plants (cts) disrupted the transport of OPDA into the peroxisome, where JA biosynthesis occurs, illuminated a critical activity of OPDA signaling in coordinating seed germination and dormancy (Russell et al, 2000). The mutant cts seeds exhibited increased accumulation level of OPDA and low germination rates (Russell et al, 2000;Dave et al, 2011), while exogenous OPDA applications stimulated the repression of the germination of WT seeds (Dave et al, 2011). Such an inhibitory effect of OPDA signaling is perhaps mediated through its activation of ABA biosynthesis by upregulating the expression of an ABA biosynthesis gene (ABA1 and ABA-deficient 1) and an inducer (RGL2, Repressor of Gibberellic Acid-like 2) of RING-H2 XERICO (ABA biosynthesis regulator) (Ko et al, 2006;Piskurewicz et al, 2008;Dave et al, 2016).…”