Download Intrinsic vs. Extrinsic signals drive development? •In animals, simpler

Intrinsic vs. Extrinsic signals drive development?
•In animals, simpler animals driven by intrinsic signals
•Signals that are contained in the cell, often arising
from factors passed down from ancestor cells
(lineage)
How to assess importance of lineage?
•Clonal analysis
•Do the same cells always have the same fate?
•More complex animals driven by extrinsic signals cell-cell signaling between neighbours (position is
critical)
•Difficult to separate in plants
Figure 3-1
Chimeric plants - sectors of genetically different cells
•Sectorial vs. periclinal
Cell killing - can one cell apt the fate of another?
•Ablate QC, procambium divides to fill QC
•Assessed by QC, procambium,columella specific markers
•suggests extrinsic rather than intrinsic
Figure 3-2
Cells of a meristematic sector are not restricted a particular fate
(e.g. leaf/not-leaf)
Cells of a meristematic layer generally give rise to particular cell
layer
Sabatini et al., 1999,
Figure 3-3
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Chimeric plants provide a situation where layer invasions can be monitored without
ablation
•Normally L1 = epidermis (no chlorophyll), L2 = subepidermis, L3 everything else
•GWG chimeras
•Fringe - L2 has adopted normally L3 fate
•Pale green - L1 (green) has invaded L2
•Therefore, layers are not always clonally distinct, but when invasions occur, cells
adopt fate according to position, not origin
Figure 3.4 Van den Berg, 1995
If kill cortical initial, pericycle cell divides periclinally to fill
cortical space
But what if consequence of ablation?
Cells are totipotent - not surprising if this pathway is induced by
laser
Colchicine induced meristematic chimeras in Datura
•Determined that cell layers usually maintain distinct lineages
•Cell sizes are very different, but co-ordination of cell division
between layers compensates
Figure 3.6 Satina et al., 1940
Figure 3.4, Stewart, 1978
Mutations that affect cell shape do not affect gross morphology
of organs
•Therefore, plant can compensate for defects in normal lineage
•Changes in cell expansion compensate for defects in division
Maize leaf
More transverse divisions
Maize leaf
Figure 3.7 Cleary and Smith, 1998
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Cell division and expansion are coordinated
•Gamma irradiating wheat embryos stops cell division,
but does not stop initiation of primordia
•Primordium is initiated by expansion of cells (cannot
form further)
fass mutants
•Cell expansion and cell division are abnormal
•Gross morphology is abnormal
•Cell fates are maintained
Figure 3.8 Foard, 1971
Figure 3.9 Torrez-Ruiz and Jurgens, 1994
Cell age and cell position are closely linked in plants
paused mutant - cell death in CZ
•slow leaf initiation, but leaf fate is not slowed
•Plant size and position of organ are changed, fate is not
•Suggests age is critical
Heterochronic - change in time of cell fate acquisition
Homeotic - change in position of cell fate acquistion
Not easy to distinguish in plants
Figure 3-10 Telfer et al., 1997
ap2-6, sepals become carpels
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altered meristem programming (amp1)
• rate of leaf initiation is increased
•Fate of leaves is like wild type at a similar age
•i.e. more leaves of each type
Psd and amp1 support the idea that age, not position,
is critical
•GAs as age monitor?
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