Abstract

Three symbiotic mutants of pea ( Pisum sativum L.) forming ineffective nodules were investigated for aberrations in nodule structure using light and transmission electron microscopy. The mutants were ordered according to the timing of the nodule development block. In the mutant RisfixO, symbiotic tissue development is arrested before the late symbiotic zone (LSZ) forms, while the infected cells of the LSZ of RisfixT lose the wild-type structure after full differentiation. In contrast to the bacteroid degradation via an electron-dense stage in RisfixO, lysis of symbiosome contents prevails in RisfixT nodules. Enhancement of the lytic function of symbiosomes in RisfixT may be interpreted in terms of the symbiosome—lysosome homology. The weakened control over symbiotic development in RisfixO may be responsible for the abundant spread of the infection threads and their enlargement. Cells from the LSZ of RisfixV undergo fast collapse, resembling defence necrosis, after differentiation. In contrast to the nodules of RisfixO and RisfixT, degraded nodules of RisfixV do not function as a sink for photosynthates and a source of the nodulation regulatory factor. This is indicated by the absence of further starch accumulation after collapse, and by hypernodulation.

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