THE PLANT CELL, Vol 5, Issue 9 1029-1038, Copyright © 1993 by American Society of Plant Biologists
LAM-1 and FAT Genes Control Development of the Leaf Blade in Nicotiana sylvestris
N. A. McHale
Department of Biochemistry and Genetics, The Connecticut Agricultural Experiment Station, New Haven, Connecticut 06504
Leaf primordia of the lam-1 mutant of Nicotiana sylvestris grow normally in
length but remain bladeless throughout development. The blade initiation
site is established at the normal time and position in lam-1 primordia.
Anticlinal divisions proceed normally in the outer L1 and L2 layers, but
the inner L3 cells fail to establish the periclinal divisions that normally
generate the middle mesophyll core. The lam-1 mutation also blocks
formation of blade mesophyll from distal L2 cells. This suggests that LAM-1
controls a common step in initiation of blade tissue from the L2 and L3
lineage of the primordium. Another recessive mutation (fat) was isolated in
N. sylvestris that induces abnormal periclinal divisions in the mesophyll
during blade initiation and expansion. This generates a blade approximately
twice its normal thickness by doubling the number of mesophyll cell layers
from four to approximately eight. Presumably, the fat mutation defines a
negative regulator involved in repression of periclinal divisions in the
blade. The lam-1 fat double mutant shows radial proliferation of mesophyll
cells at the blade initiation site. This produces a highly disorganized,
club-shaped blade that appears to represent an additive effect of the lam-1
and fat mutations on blade founder cells.
