SHI was cloned by
Fridborg et al. (2001). See
also Fridborg et al., 1999.
SHI function is unknown, but it may be a
transcription factor: Among other features, it contains
a Zn finger and 2 putative nuclear localization
SHI is normally expressed in young organs,
but in the WT, the SHI transcript was not detected.
SHI is a negative
regulator of the GA transduction pathway:
The shi mutants were
first obtained by transposon mutagenesis. They are dwarf
and flower late, and resemble
gai mutants. They also
contain high levels of GAs, but are insensitive to GAs.
This phenotype is semi-dominant.
In the shi
mutants, SHI is over-expressed. When SHI
is over-expressed under the control of the 35S promoter, the
resulting phenotype is the same as in the shi
mutants. SHI is therefore a
negative regulator of the GA response.
However, the loss of SHI
function give no apparent phenotype. As SHI belongs to a
multigene family, its function may be complemented by other genes
in the family.