This investigation confirmed that plant reaction to Al was
directed through the disruption of intercellular co-ordination existing
between the cell populations comprising the root meristem.
The first detectable response to A1 in the root involved
disruption of Golgi apparatus function in the cap periphery.
Ultrastructural changes in the cap periphery coincided with the presence
of A1 in these cells. Conspicuous physiological changes involving cell
enlargement, cell metabolism and root elongation were identified in cells
initially remote from the site(s) of A1 uptake. Communication between
A1-damaged peripheral root cap cells and the cell populations of the cap
and proximal meristems, quiescent centre and region of cell growth
was therefore indicated. A decrease in amyloplast numbers in response
to increasing AI concentration coincided with diminished Golgi apparatus
activity in the peripheral cap. These changes preceded detectable
reductions in mitotic activity, indicated by decreases in cap volume and
root length, and it was consequently suggested that control of intercellular
activities in the root meristem may be directed through
polysaccharide metabolism.
Low concentrations of A1 (≤ 1,25 mg dm ¯³) produced a positive
growth response in the primary root. This coincided with an increase in
mean cap volume and these events were interpreted as an A1-induced
release of the proximal meristem from growth inhibition originating in
the cap. Experiments which followed the effect of decapping on the
morphology of quiescent centre cells in the presence and absence of A1
supported the existence of a Golgi apparatus-derived morphogen involved
in the control of Golgi apparatus secretory activity and plastid
differentiation. In contrast to the controls (0 ABA). treatment of
decapped roots with 2 X 10[-4] and 5 X 10[-5] M abscisic acid inhibited the
development of Golgi apparatus secretory activity and plastid
differentiation. It is postulated therefore, that an early response to
AI may involve inhibition of the basipetal movement of an endogenous
growth inhibitor originating in the cap, which may be ABA. The presence of A1 in the nutrient solution caused an efflux of
H[+] from the root. Some of the more adverse plant responses to AI were
initiated at A1 concentrations where the molar ratio of charge between
Ca[2+] and A1[3+] favoured A1. An hypothesis for an electrophysiological
plant response to A1 involving membrane hyperpolarisation by Al ions is
developed.
Chemical analysis of plant fractions did not connect
A1-induced nutrient disorders with the primary expression of A1 toxicity. / Thesis (Ph.D.)-University of Natal, Pietermaritzburg, 1986.
| Identifer | oai:union.ndltd.org:netd.ac.za/oai:union.ndltd.org:ukzn/oai:http://researchspace.ukzn.ac.za:10413/10525 |
| Date | January 1986 |
| Creators | Bennett, Robin John. |
| Contributors | Breen, Charles M. |
| Source Sets | South African National ETD Portal |
| Language | English |
| Detected Language | English |
| Type | Thesis |
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