Seed germination is antagonistically controlled by the phytohormones gibberellic acid (GA) and abscisic acid (ABA). GA promotes seed germination by enhancing the proteasome-mediated destruction of RGL2 (for RGA-LIKE2), a key DELLA factor repressing germination. By contrast, ABA blocks germination by inducing ABI5 (for ABA-INSENSITIVE5), a basic domain/leucine zipper transcription factor repressing germination. Decreased GA synthesis leads to an increase in endogenous ABA levels through a stabilized RGL2, a process that may involve XERICO, a RING-H2 zinc finger factor promoting ABA synthesis. In turn, increased endogenous ABA synthesis is necessary to elevate not only ABI5 RNA and protein levels but also, critically, those of RGL2. Increased ABI5 protein is ultimately responsible for preventing seed germination when GA levels are reduced. However, overexpression of ABI5 was not sufficient to repress germination, as ABI5 activity requires phosphorylation. The endogenous ABI5 phosphorylation and inhibition of germination could be recapitulated by the addition of a SnRK2 protein kinase to the ABI5 overexpression line. In sleepy1 mutant seeds, RGL2 overaccumulates; germination of these seeds can occur under conditions that produce low ABI5 expression. These data support the notion that ABI5 acts as the final common repressor of germination in response to changes in ABA and GA levels.

Seed dormancy is an ecologically important adaptive trait in plants whereby germination is repressed even under favorable germination conditions such as imbibition with water. In Arabidopsis and most plant species, dormancy absolutely requires an unidentified seed coat germination-repressive activity and constitutively higher abscisic acid (ABA) levels upon seed imbibition. The mechanisms underlying these processes and their possible relationship are incompletely understood. We developed a "seed coat bedding" assay monitoring the growth of dissected embryos cultured on a layer of seed coats, allowing combinatorial experiments using dormant, nondormant, and various genetically modified seed coat and embryonic materials. This assay, combined with direct ABA measurements, revealed that, upon imbibition, dormant coats, unlike nondormant coats, actively produce and release ABA to repress embryo germination, whatever the embryo origin, i.e., from dormant, nondormant, or never dormant aba seeds, unable to synthesize ABA. The persistent high ABA levels in imbibed dormant seeds requires the permanent expression of the DELLA gene RGL2, where it remains insensitive to gibberellins (GA) unlike in nondormant seeds. These findings present the seed coat as an organ actively controlling germination upon seed imbibition and provide a framework to investigate how environmental factors break seed dormancy.gibberellins | seed dormancy | DELLA | seed germination | ABI5

Formation of singlet oxygen ( 1 O 2 ) has been implicated with damaging photosystem II (PSII) that needs to undergo continuous repair to maintain photosynthetic electron transport. In addition to its damaging effect, 1 O 2 has also been shown to act as a signal that triggers stress acclimation and an enhanced stress resistance. A signaling role of 1 O 2 was first documented in the fluorescent (flu) mutant of Arabidopsis. It strictly depends on the chloroplast protein EXECUTER1 (EX1) and happens under nonphotoinhibitory light conditions. Under severe light stress, signaling is initiated independently of EX1 by 1 O 2 that is thought to be generated at the acceptor side of active PSII within the core of grana stacks. The results of the present study suggest a second source of 1 O 2 formation in grana margins close to the site of chlorophyll synthesis where EX1 is localized and the disassembly of damaged and reassembly of active PSII take place. The initiation of 1 O 2 signaling in grana margins depends on EX1 and the ATP-dependent zinc metalloprotease FtsH. As FtsH cleaves also the D1 protein during the disassembly of damaged PSII, EX1-and 1 O 2 -mediated signaling seems to be not only spatially but also functionally associated with the repair of PSII.

Under the canopy, far-red (FR) light represses seed germination by inactivating phytochrome photoreceptors. This elicits a decrease in gibberellins (GA) levels and an increase in abscisic acid (ABA) levels. GA promotes germination by enhancing the proteasome-mediated destruction of DELLA repressors. ABA prevents germination by stimulating the expression of ABI repressors. How phytochromes elicit changes in hormone levels or how GA-and ABA-dependent signals are coordinated to repress germination remains poorly understood. We show that repression of germination by FR light involves stabilized DELLA factors GAI, RGA and RGL2 that stimulate endogenous ABA synthesis. In turn, ABA blocks germination through the transcription factor ABI3. The role of PIL5, a basic helix-loop-helix transcription factor stimulating GAI and RGA expression, is significant, provided GA synthesis is high enough; otherwise, high GAI and RGA protein levels persist to block germination. Under white light, GAI and RGA driven by the RGL2 promoter can substitute for RGL2 to promote ABA synthesis and repress germination, consistent with the recent findings with RGL2. The three DELLA factors inhibit testa rupture whereas ABI3 blocks endosperm rupture.