Although the Arabidopsis thalianagenome contains more than 90 J-domain genes
(Miernyk 2001), only two encode proteins that are similar to ARG1 throughout their
lengths: ARG1-Like 1 (ARL1) and ARL2. A reverse genetic approach was used to
demonstrate that ARL2 also contributes to early phases of gravity signal transduction,
whereas ARL1 does not. In fact, physiological and molecular studies of arl2mutant
seedlings also showed defects in lateral auxin transport and PIN3 protein relocalization
within the root statocytes upon gravistimulation (Guan et al. 2003; Harrison and Masson
2006). Hence, ARG1 and ARL2 appear to function in the same pathway. In agreement
with this conclusion, arg1-2 arl2-1 double mutants show intermediate gravitropic defects
that are similar to those of the corresponding single mutants (Guan et al. 2003).
Analysis of double mutants between arg1-2, arl2-1, andpgm-1also led to surprising
results. Remember that pgm-1affects phosphoglucomutase, an enzyme that contributes
to starch biosynthesis. As discussed above, both pgm-1andarg1-2orarl2-1display al-
tered kinetics of gravitropism. However, their gravitropic defects are not complete and
their organs still develop reasonably strong gravitropic responses, though with slower ki-
netics. If PGMandARG1/ARL2contribute to a linear gravity signal transduction path-
way in the statocytes, double mutants should display a phenotype similar to that of sin-
gle mutants.
Whenarg1-2 pgm-1andarl2-1 pgm-1double mutants were analyzed, a surprisingly
strong enhancement of the gravitropic defect was observed relative to that of single mu-
tants (Boonsirichai et al., unpublished data; Guan et al. 2003). This result can be ex-
plained in several ways. First, it is possible that ARG1andARL2function in a pathway
that is distinct from the PGM pathway. In fact, as discussed in Chapter 1, several exper-
iments have suggested the existence of more than one mechanism of gravity sensing in
roots. Second, it is possible that these mutations affect partially their respective steps in
a linear pathway. Indeed, ARG1has been postulated to function as part of a chaperone
complex that might modulate, but not be required for, the targeting or activity of
membrane-associated proteins in the statocytes, whereas pgm-1mutants are not com-
pletely defective in amyloplast sedimentation (Saether and Iversen 1991).
In addition to revealing the possible topology of the gravisensing network, these
double-mutant studies suggest alternative genetic strategies to search for novel gravity
signal transducers. For instance, a screen for genetic enhancers of arg1-2/arl2-3may lead
to the identification of new gravity signal transducers in the “PGMgenetic pathway,”
whereas searching for enhancers of pgmwill likely lead to the discovery of genes that
function in the “ARG1/ARL2genetic pathway.” The recent isolation and initial character-
ization of mutations falling in the first group (genetic enhancers of arg1-2) allowed the
identification of an outer plastid membrane-associated protein as a possible gravity sig-
nal transducer, boding well for the success of this approach (Stanga et al. 2006).
Genetic studies have also been quite effective at uncovering gravity signal transducers
in aboveground organs through careful investigations of Arabidopsismutants with de-
fects in shoot gravitropism. As discussed in Chapter 1, a number of shoot gravitropism
(sgr) mutants have been identified in Arabidopsiswhich exhibit reduced gravitropic re-
sponses in inflorescence stems (Yamauchi et al. 1997). Several of these mutants have
been very useful for our understanding of gravity perception in shoots as they confirmed
endodermal cells as shoot statocytes, re-emphasized the contribution of amyloplast sedi-
frankie
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