Arbuscular mycorrhiza development in pea (Pisum sativum L.) mutants impaired in five early nodulation genes including putative orthologs of NSP1 and NSP2

作者:Shtark Oksana Y*; Sulima Anton S; Zhernakov Alexander I; Kliukova Marina S; Fedorina Jaroslava V; Pinaev Alexander G; Kryukov Alexey A; Akhtemova Gulnara A; Tikhonovich Igor A; Zhukov Vladimir A
来源:Symbiosis, 2016, 68(1-3): 129-144.
DOI:10.1007/s13199-016-0382-2

摘要

Arbuscular mycorrhiza (AM) development in five non-nodulating pea (Pisum sativum L.) mutants (sym7, sym11, sym14, sym34, sym38) grown in nurse pots was analyzed at the early stages of colonization by Rhizophagus irregularis. Abundance of external mycelium attached to the root surface and parameters of internal fungal colonization, i.e. intensity of colonization, and arbuscule and vesicle/spore abundance, were evaluated. Mutations in SYM7 (putative ortholog of NSP2, 'nodulation signaling pathway 2'), SYM11, and SYM14 genes resulted in considerable increase in root surface colonization and a substantial decrease in internal colonization as compared to corresponding wild-type pea lines (wt). In addition, the mutants sym7 and sym11 displayed a highly reduced amount of arbuscules. In contrast, plants mutated for the SYM34 gene displayed strongly reduced root surface colonization. The mutant sym34 also had strongly reduced internal colonization after 10 days of growth, but did not differ from wt 10 days later. The sym38 mutant did not differ from wt. These data indicate that all pea genes analyzed, except SYM38, are essential for both nodule and AM development. The phenotype of sym34 suggested that the pea SYM34 gene is an ortholog of the Medicago truncatula NSP1 ('nodulation signaling pathway 1'), and early stop codons were in fact detected in an NSP1 homologous sequence of two sym34 mutants. In addition, full co-segregation of the allelic states of a molecular marker representing a polymorphic fragment of the hypothetical pea NSP1 gene, together with the nodulation phenotype of 50 F-2 plants, support our hypothesis. A possible explanation for the different AM phenotypes of sym7 and sym34 is given.

  • 出版日期2016-3