5.1 ǀ Phosphorus
Severe P deficiency is uncommon in lowland rice on young alluvial paddy
soils because the soil P reserves are solubilized in reductive
dissolution reactions following soil submergence, and the P is therefore
readily-available to the crop. It is much more common in
highly-weathered soils of inland valleys (Figure 1), which typically
have very low extractable P contents. Phosphorus deficiency interacts
with Fe toxicity in various ways, tending to exacerbate the direct
effects (Sahrawat, 2005). Phosphorus deficiency causes delayed
phenological development in rice by up to a month (Dobermann &
Fairhurst, 2000; Vandamme et al., 2018). In soils for which the Fe toxic
conditions develop very slowly following submergence, delayed phenology
may mean late season exposure to the stress that is otherwise be
avoided. On the other hand, under chronic low-level exposure in acid
sandy soils, slower growth might mean less Fe is accumulated in the
plants and they have longer to acclimatise to it.
Phosphorus deficiency typically results in increased root: shoot ratios,
and increased root surface area means increased exposure to
Fe2+. Kirk & Du (1997) found P deficiency in
deoxygenated nutrient culture caused increased primary root porosity and
an increased proportion of fine lateral roots compared to P-sufficient
plants, resulting in in two-fold greater rates of O2release per plant. Under Fe toxic conditions this could compensate for
the greater exposure to Fe2+. Likewise, Fu, Yang &
Shen (2014) found greater root oxidizing capacity under P deficiency.
Phosphorus deficiency also results in impaired cell membrane integrity
and therefore loss of organic substrates into the rhizosphere (Rose et
al., 2013). This may fuel re-reduction of Fe(OH)3previously oxidized by O2 release from the root tip
zone, so exacerbating Fe2+ toxicity (Benckiser et al.,
1984).