Environmental Engineering Reference
In-Depth Information
antioxidants. An alternative mechanism may be the induction by UV-B of proteases
specific to the proteins that are degraded. It is possible that UV-B is inducing such a
senescence-like response, as has been implicated in plant responses to tropospheric
ozone where specific proteins are degraded that are spatially separated from the site of
primary oxidative damage
22
.
In contrast, when plants were developed from seed under high UV-B doses, there
were no effects on photosynthesis (Table I
14
). A likely protective mechanism is an
increase in the content of UV-B-absorbing compounds (i.e. flavonoids) found in these
irradiated plants. The induction of UV-B-absorbing compounds in leaves is one of the
best-described and most widespread responses of plant to UV-B.
Stomata
Changes in stomatal function play a major role in the UV-B-induced inhibition
of CO
2
assimilation. Sudden exposure of pea plants to high UV-B doses largely
decreases both adaxial and abaxial g
s
(Table I
15
). However, when plants were grown and
developed under UV-B for 24 d in a greenhouse, adaxial g
s
was substantial decreased,
with no major effects on abaxial g
s
15
. The effects on adaxial g
s
were mediated by
changes in aperture, as there was no reduction in stomatal density in these pea leaves.
The adaxial stomata are the cells that are most exposed to UV-B radiation, because they
are not screened by flavonoids in the epidermal layer.
It is clear that there is a direct effect of UV-B on stomata in addition to that
caused by changes in the mesophyll photosynthesis of the leaves:
(i) the effects on adaxial g
s
on plants grown and developed under UV-B for 24 d in a
greenhouse were accompanied by no changes in any photosynthetic parameter
measured
(ii) the effects of UV-B was largest on the exposed adaxial leaf surface (if UV-B was
affecting mesophyll photosynthesis it presumably would have affected both leaf
surfaces equally)
(iii) when leaves were inverted the light level on the different epidermis is changed by
10-50 fold, but photosynthesis should not be affected as the same total photon flux
density is incident on the mesophyll. Therefore, we expected that the so-called
“direct” response of guard cells to light, which acts independently of the response
to
c
i
or to some mesophyll photosynthesis-related signal, would result in abaxial
stomata opening and adaxial stomata closing. This was exactly what was observed
in the control plants. In the UV-B treatments the opening response of abaxial
stomata on inversion was either reduced or eliminated at highest dose, while the
adaxial stomata (with a lower sensitivity to light) closed.
The mechanism for the UV-B effect on stomata is not clear. One potential
mechanism is an inhibition of ATP synthesis by electron transport in guard cells
thylakoids. A second mechanism may involve a direct inhibition by UV-B of the
plasmalemma ATPase proton pump
1
. Alternatively, UV-B may not directly affect the
generation of the guard cell turgor pressure, but rather the effect of this turgor on pore
size through UV-B-induced changes in the elasticity of the cell walls or cytoskeleton of
guard cells and the neighbouring epidermal cell. This possibility warrants further
investigation.
Search WWH ::
Custom Search