AI Article Synopsis
- The study compares three pea mutants with defects in nodule development to understand how these abnormalities affect nodule morphogenesis.
- Wild-type plants successfully develop nodules by allowing cell proliferation, while two mutants, RisFixA and SGEFix–-2, get stuck at an early stage without proper cell types, indicating the need for certain cells for complete nodule formation.
- In a third mutant, SGEFix–-1, nodule development initially follows the wild type but fails later, leading to a proposed sequential interaction of specific symbiotic genes (Sym33, Sym40, Sym41) crucial for nodule formation.
Article Abstract
A comparative analysis of nodule morphogenesis was carried out for three symbiotically defective pea (Pisum sativum) mutants that show abnormalities in nodule development.In the wild-type lines, resumption of cell proliferation in the pericycle and inner cortex results in the development of a nodule primordium, within which are found proliferating cells that harbour infection threads. However, this class of cell is not observed in the mutants RisFixA (sym41) and SGEFix–-2 (sym33) where nodule development is arrested at the point of formation of the apical nodule meristem. Itis proposed that the presence of proliferating cells harbouring infection threads is a prerequisite for normal formation of the nodule meristem.In mutant SGEFix–-1 (sym40), nodule development does not differ from that of wild-type plants in the early stages but is blocked at the stage after nodule meristem persistence. A scheme is proposed for the sequential functioning of pea symbiotic genes Sym33, Sym40 and Sym41 in the programme of nodule development.
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| http://dx.doi.org/10.1111/j.1469-8137.2008.02723.x | DOI Listing |
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