Agriculture Reference
In-Depth Information
Loss-of-function mutations in
KN1
and its functional orthologue in
Arabidopsis
,
SHOOT MERISTEMLESS
(
STM
), are characterised by a failure to develop and/or
maintain a shoot apical meristem (Barton & Poethig, 1993; Clark
et al.
, 1996; En-
drizzi
et al.
, 1996; Long
et al.
, 1996; Kerstetter
et al.
, 1997; Vollbrecht
et al.
, 2000).
As both
stm
and
wus
mutants impart similar mutant phenotypes, their functional
relationship has been the focus of several studies. Genetic analysis places
WUS
downstream of
STM
(Endrizzi
et al.
, 1996), which is consistent with an inability to
maintain
WUS
expression in developing
stm
mutant embryos (Mayer
et al.
, 1998).
However, this hierarchy of gene activity is at odds with the observation that
WUS
is
expressed before
STM
in embryogenesis (Long & Barton, 1998; Mayer
et al.
, 1998).
The precise regulatory relationship between
STM
and
WUS
has therefore been dif-
ficult to determine. Using slightly different approaches, several recent studies have
shown that
STM
and
WUS
regulate distinct genetic pathways (Brand
et al
., 2002;
Gallois
et al
., 2002; Lenhard
et al
., 2002). For instance ectopic expression of
STM
in
organs promotes the expression of several other
KNOX
genes but not
CLV3
, whereas
CLV3
is detected in organs expressing
WUS
(Lenhard
et al.
, 2002). Ectopic expres-
sion of both
WUS
and
STM
in organs has a synergistic effect, resulting in elevated
levels of
CLV3
expression (Brand
et al.
, 2002; Gallois
et al.
, 2002; Lenhard
et al.
,
2002). Based on these observations it has been proposed that one function of
STM
is to prevent cell differentiation within the meristem, rather than directly promoting
stem cell identity (Lenhard
et al.
, 2002).
WUS
on the other hand promotes stem
cell identity, but in the absence of
STM
, these cells eventually differentiate. Thus
the combined activity of
STM
and
WUS
is required to maintain a self-perpetuating
population of stem cells. However, although meristem-like structures arise from or-
gans expressing both
STM
and
WUS
, they do not develop into fully formed shoots,
suggesting that other factors are required for meristem maintenance (see Tables 6.1
and 6.2).
STM
maintains stem cell fate in part by restricting the expression of the MYB-
domain transcription factor
ASYMMETRIC LEAVES1
(
AS1
) and the leucine zipper
domain transcription factor
AS2
to organ founder cells and primordia in the periphery
of the meristem. Presence of both
AS1
and
AS2
transcript throughout the apex of
stm
mutant embryos suggests that the failure to develop a meristem may be a direct
consequence of
AS1
and
AS2
misexpression (Byrne
et al.
, 2000, 2002; Iwakawa
et al.
,
2002). This was elegantly demonstrated by showing that
as1 stm
and
as2 stm
double
mutants form functional meristems (Byrne
et al.
, 2000, 2002). One of the functions
of
AS1
and
AS2
is to prevent
KNOX
gene expression in incipient organ primordia.
Both
as1
and
as2
mutants have lobed leaves that are similar in appearance to the
leaves of plants constitutively expressing the
KNOX
gene,
BREVIPEDICELLUS
(Lincoln
et al.
, 1994; Byrne
et al.
, 2000; Ori
et al
., 2000; Semiarti
et al.
, 2001).
Transcripts of several
KNOX
genes were subsequently found to accumulate in
as1
and
as2
leaves, suggesting the leaf phenotype is caused by ectopic
KNOX
expression
(Ori
et al.
2000; Semiarti
et al.
, 2001). The similarity between
as1
and
as2
mutant
phenotypes implies that they may function in a common pathway to regulate
KNOX
expression. Consistent with this model is the recent finding that AS1 and AS2
proteins physically interact
in vitro
, suggesting they may form a complex
in planta
