Regulation of flowering time in Arabidopsis



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Flowering pathway

Gibberellin pathway



The Gibberellin transduction pathway


SLY1 (SLEEPY 1) (also: GAR2)


The SLY1 gene contains no introns and encodes a predicted protein of 151 amino-acids (McGinnis et al., 2003).

SLY1 is an F-box protein. It is presumably a sub-unit of an SCF E3 ubiquitin ligase complex involved in protein degradation. In this kind of complex, the F-box protein binds to the rest of the complex via the F-box domain, and interacts through its C-terminus with a specific protein targeted for ubiquitination, which will be later degraded by the 26S proteasome (McGinnis et al., 2003; Fu et al., 2004; see also the review by Sun and Gubler, 2004).

The C-terminus domain of SLY1 is a protein-protein interaction domain. It is necessary for the SLY1 function, as both sly1-2 and sly1-10 loss-of-function mutant alleles have an intact F-box, but lack the C-terminal domain (McGinnis et al., 2003).

Transient expression assays (GUS fusions in epidermal cells) show that the SLY1 protein is present in the nucleus, although no nuclear localization motifs have been identified by sequence analysis (Dill et al., 2004).

SLY1 expression:

  • SLY1 is expressed, at low levels, in all the tissues examined: rosette and cauline leaves, stem, flowers, siliques and seedlings (Mc Ginnis et al., 2003).

  • In the WT, SLY1 expression is not significantly modified after GA treatment (Dill et al., 2004).

SLY1 over-expression:

  • Plants over-expressing SLY1 (under the control of the 35S promoter) have no obvious phenotype. However, they are more resistant to the GA-synthesis inhibitor, paclobutrazol (PAC) (Fu et al., 2004).
  • SLY1 over-expression suppresses the phenotype conferred by the sly1-10 loss-of-function mutation, as well as the gai-t6 and ga1-3 loss-of-function mutations (Fu et al., 2004).
  • Over-expression of the sly1-2 loss-of-function allele (controlled by the 35S promoter) makes the plants dwarf and late-flowering. The intensity of the phenotype is correlated with the level of sly1-2 expression (Strader et al., 2004).

Antisense expression of SLY1

Surprisingly, the plants expressing an antisense SLY1 transcript have no apparent phenotype. In the sly1-2 and sly1-10 backgrounds, though, the antisense SLY1 complements the mutant phenotype (Strader et al., 2004). What happens is that another gene (SNE) has a redundant role with SLY1, and can complement the loss of SLY1 function only in the absence of any sly1 transcript (See also here).


Two groups of sly1 mutants have been characterized: the loss-of function mutants, such as sly1-10 and sly1-2, and the gain-of-function (or modification-of-function) mutants, such as sly1-d.

  • Loss-of-function mutants:

The sly1 loss-of-function mutants have been isolated through a screen for suppressors of the abi1-1 mutation, allowing the seeds to germinate in presence of ABA. However, the sly1 mutants are also only able to germinate in the presence of the abi1-1 mutation (Steber et al., 1998).

The sly1 loss-of-function mutants have the general phenotype of GA response mutants, including short size, dark green leaves, and late-flowering. They resemble the ga1-3 phenotype and are mostly insensitive to GAs(Steber et al., 1998; Steber and McCourt, 2001; Dill et al., 2004). These mutations are recessive.

The sly1-1 to sly1-5 mutants have been isolated by Steber et al. (1998). Among them, sly1-1 seems to be the weakest allele.

In the sly1-2 mutant allele,  a deletion of 2 base pairs causes a frameshift. As a consequence, the last 40 amino-acids in the protein are missing, and this affects the C-terminus domain (Mc Ginnis et al., 2003).

The sly1-10 mutant was reported by Steber and McCourt (2001). The sly1-10 mutant allele has a 23 bp deletion in the coding sequence, followed by an insertion of 8 kb. This results in the loss of the last 8 amino-acids in the protein, and the addition of 46 random amino-acids at the C-terminus of the protein. The gene is still expressed in this mutant (Mc Ginnis et al., 2003).

  • The sly1-d gain-of-function mutant (a.k.a gar2-1):

The sly1 gain-of-function mutants have a completely different phenotype than the sly1 loss-of-function mutants, as they flower early, both in long days and in short days (the effect is however more pronounced in SD). These mutants over-accumulate GAs (Peng et al., 1999(1)).

The gar2-1 mutant was isolated through a screen for suppressors of the gai mutant phenotype. It is a dominant mutation (Wilson and Somerville, 1995). This mutant was later identified as a SLY1 gain-of-function mutant allele, and re-named sly1-d (Dill et al., 2004). In the WT background, however, gar2-1 has no obvious mutant phenotype, other than its ability to germinate in presence of Paclobutrazol (Peng et al., 1997), indicating that the gar2-1 mutation lowers the requirement for GAs.

The sly1-d allele has a point mutation, which results in a single amino-acid substitution in the C-terminal domain of the protein (in the LSL domain, a highly conserved motif among several F-box proteins in Arabidopsis) (Dill et al., 2004; Fu et al., 2004).


Interaction between GAs, the SLY1 protein and RGA or GAI (DELLA) proteins: