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(away from the meristem) axis. A connection between the ad-abaxial patterning
of a lateral organ and the shoot apical meristem was first established by surgical
experimentation (Sussex, 1955; Snow & Snow, 1959; Hanawa, 1961). When an
incision or impermeable barrier was placed between a young organ primordium and
the meristem, formation of adaxial cells was impaired and the resulting organ had a
radial symmetry (i.e. needle-like). These findings gave the first tantalising evidence
that a meristem-derived signal promotes adaxial cell identity in developing organs.
In addition, it showed that abaxial cells form in the absence of adaxial cells and
that the presence of adaxial cell types was required for lateral growth, as in their
absence organs failed to form a lamina. Similar surgical treatment to slightly older
primordia had no affect on adaxial cell identity and leaf morphology, suggesting
that there is only a transitory requirement for the meristem signal during the early
stages of organ development.
Supporting evidence for a meristem-derived adaxialising morphogen comes from
the characterisation of gain-of-function mutations in two closely related Arabidopsis
genes, PHABULOSA ( PHB ) and PHAVOLUTA ( PHV ). These mutations cause a
dose-dependent adaxialisation of organs, with severely affected organs having a
needle-like morphology when abaxial cell types fail to form (McConnell & Barton,
1998). The loss of lateral growth when either adaxial or abaxial cells are missing
from a developing organ implies that signalling between these cell types may be
required to initiate lateral growth at the point where they meet, as first proposed by
Waites and Hudon (1995). PHB and PHV belong to a family of likely transcription
factors with homeodomain, leucine zipper and START domain motifs ( HD-ZIP ). The
gain-of-function mutations affecting PHB and PHV arise from nucleotide changes
in a small region of the START domain, a motif that has been implicated in the
binding of sterol lipid ligands in a number of diverse proteins (McConnell et al. ,
2001). This raises the possibility that PHB and PHV proteins are activated by a
meristem-derived sterol, which is presumably more abundant in the adaxial domain
(side closest to the meristem) than the abaxial domain of the incipient primordium.
It has been proposed that the proteins encoded by the dominant phb and phv mutant
alleles are constitutively active and are no longer responsive to the meristem-derived
signal. The accumulation of phb and phv transcripts in the abaxial domain of mutant
organs is consistent with activated PHB and PHV proteins promoting their own
RNA as well as adaxial cell identity (McConnell et al. , 2001).
Normally PHB and PHV expression is restricted to the adaxial domain, although
within this domain there is a gradient of expression, with the strongest expression
being closest to the meristem. The gradient of PHB and PHV expression, and by
inference activation, may therefore reflect the gradient of activating signal from the
meristem. Similarly, accumulation of PHB and PHV transcripts in narrow strips
that extend from the initiating organ into the centre of the meristem might also
reflect the likely path of the signal. Based on these observations it is tempting to
speculate that the signal promoting PHB and PHV activation is the same as that
identified in the surgical experiments. It is produced in the centre of the meristem
and flows towards the periphery forming a concentration gradient, with adaxial
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