Comparative transcriptomics reveals suppressed expression of genes related to auxin and the cell cycle contributes to the resistance of cucumber against Meloidogyne incognita

Abstract

Background: Meloidogyne incognita is a devastating nematode that causes significant losses in cucumber production worldwide. Although numerous studies have emphasized on the susceptible response of plants after nematode infection, the exact regulation mechanism of M. incognita-resistance in cucumber remains elusive. Verification of an introgression line, 'IL10-1', with M. incognita-resistance provides the opportunity to unravel the resistance mechanism of cucumber against M. incognita. Results: In the present study, analyses of physiological responses and transcriptional events between IL10-1 (resistant line) and CC3 (susceptible line) were conducted after M. incognita infection. Physiological observations showed abnormal development of giant cells and M. incognita in IL10-1, which were the primary differences compared with CC3. Furthermore, Gene ontology (GO) analysis revealed that genes encoding cell wall proteins were up-regulated in IL10-1 and that the highly expressed lipid transfer protein gene (Csa6G410090) might be the principal regulator of this up-regulation. Simultaneously, analyses of gene expression profiles revealed more auxin-related genes were suppressed in IL10-1 than in those of CC3, which corresponded with the lower level of indole acetic acid (IAA) in the roots of IL10-1 than in those of CC3. Additionally, poor nucleus development as a clear indication of abnormal giant cells in IL10-1 was related to inhibition of the cell cycle. Of those genes related to the cell cycle, the F-box domain Skp2-like genes were down-regulated in IL10-1, whereas more of these genes were up-regulated in CC3. Conclusions: All of these findings indicate that suppressed expression of genes related to auxin and the cell cycle and highly expressed cell wall proteins play important roles in the abnormal development of giant cells, which hinders the development of M. incognita, thereby causing resistance to M. incognita in IL10-1. Knowledge from this research will provide a useful foundation for developing effective strategies in M. incognita-resistance breeding.