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Anatomical variation of mesophyll conductance under potassium deficiency has a vital role in determining leaf photosynthesis
Author(s) -
Lu Zhifeng,
Lu Jianwei,
Pan Yonghui,
Lu Piaopiao,
Li Xiaokun,
Cong Rihuan,
Ren Tao
Publication year - 2016
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/pce.12795
Subject(s) - photosynthesis , potassium deficiency , chloroplast , cultivar , brassica , conductance , biology , cytoplasm , potassium , botany , stomatal conductance , chemistry , microbiology and biotechnology , biochemistry , gene , mathematics , organic chemistry , combinatorics
Abstract Leaves exposed to potassium (K) deficiency usually present decreased mesophyll conductance ( g m ) and photosynthesis ( A ). The relative contributions of leaf anatomical traits in determining g m have been quantified; however, anatomical variabilities related to low g m under K starvation remain imperfectly known. A one‐dimensional model was used to quantify anatomical controls of the entire CO 2 diffusion pathway resistance within a leaf on two Brassica napus L. cultivars in response to K deficiency. Leaf photosynthesis of both cultivars was significantly decreased under K deficiency in parallel with down‐regulated g m . The mesophyll conductance limitation contributed to more than one‐half of A decline. The decreased internal air space in K‐starved leaves was associated with the increase of gas‐phase resistance. Potassium deficiency reduced liquid‐phase conductance by decreasing the exposed surface area of chloroplasts per unit leaf area ( S c / S ), and enlarging the resistance of the cytoplasm that can be interpreted by the increasing distance of chloroplast from cell wall, and between adjacent chloroplasts. Additionally, the discrepancies of A between two cultivars were in part because of g m variations, ascribing to an altered S c / S . These results emphasize the important role of K on the regulation of g m by enhancing S c / S and reducing cytoplasm resistance.