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).