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Fig. 6. The effects of LHW on RM establishment and maintenance. (A-P)
Expression of meristem markers (green) in wild-type (WT) and lhw-1
7-dpg seedlings. (A,B) SCR::GFP expression; (C) SCR::GFP
expression in a torpedo-stage lhw-1 embryo; (D,E) columella
differentiation marker Q1630::GFP expression; (F,G) CYCB1;2::GUS expression;
(H-P) QC25::GUS (blue) and starch granules (purple) mark the degeneration of
the lhw meristem over time (H-I, 7 dpg; J-L, 13 dpg; M-P, 18 dpg).
(L) Higher-magnification image of K; star indicates starch-granule-containing
cells adjacent to QC25-marked cells. (N) Higher-magnification image of M. For
each marker, the wild-type and lhw image pair are at the same
magnification. Arrows point to quiescent center (QC) cells. (Q) Graph
of wild-type (dark grey) and lhw-1 (light grey) root growth over
time. Error bars ±s.e.m. (R) Model for LHW action in generating
vascular pattern. LHW is required to establish the radial extent of
the root vascular tissues in the embryo and promotes postembryonic divisions
in these tissues. LHW therefore acts as a meristem size-control protein for
the center of the root. LHW and WOL are both required for
these cell divisions, but appear to act at least somewhat independently. We
propose that the eventual slowing down of longitudinal growth in lhw
mutant roots is not due to a direct requirement for LHW in meristem
maintenance, but because LHW is required to create the tissue that
normally produces SHR. Without adequate levels of SHR, SCR is not maintained
in the QC and meristems eventually terminate. Scale bars: 30 µm.
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