Remediation of Pear Iron Deficiency Chlorosis by Nanocellulose-iron Chelation and the Underlying Mechanism

Abstract

Nanocrystal cellulose possesses a strong capability to chelate Fe due to its adsorptive properties. Iron deficiency chlorosis (IDC) is a mineral disorder that remarkably weakens pear photosynthesis, causing declines in plant yields and quality. Conventional methods for controlling IDC generally lack efficiency and overuse chemicals. Foliar application of nanocellulose (NC)-Fe chelate (NCFe) provides a new approach to remediate IDC in pear (Pyrus betulifolia). In this study, NC was prepared by acidic hydrolysis using 64 wt% H2SO4 at 45 °C for 45 minutes. NCFe was formulated based on the net charge density of NC and ferrous sulfate (FeSO4) solution. The nanoparticle properties were characterized by transmission electron microscopy (TEM), dynamic light scattering, and conductometry. Pyrus betulifolia seedlings were pre-etiolated in an improved Hoagland’s nutrient solution and treated with bicarbonate. Changes in chlorophyll content, active Fe content, and photosynthesis rate in NCFe-treated leaves were determined by SPAD values, spectrophotometry, and photosynthetic apparatus, respectively. Ferritin genes (PbFER) and pectin methylesterase genes (PbPME) were extracted from leaf tissue, and gene expression profiles were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The results showed that NCFe particles maintained a whisker-like morphology; the Z-average hydrodynamic diameter and zeta potential of NCFe measured by dynamic light scattering were 107.4 ± 3.0 nm and −9.7 ± 0.4 mV, respectively. When NCFe was prepared at a mixing ratio of 1:3000, the total chlorophyll content, active Fe content, and net photosynthetic rate of plant leaves were significantly enhanced by 23.8%, 65.9%, and 40.4% after 72 hours of treatment, respectively, compared with FeSO4 spraying. Importantly, NCFe treatment also significantly downregulated the expression of PbPME and upregulated the expression of PbFER, which are key genes regulating the active Fe content.