INTRODUCTION Parasitic nematodes are infectious and damaging pests for the majority of cultivars, and they inflict huge yield losses. The annual and cumulative damage to world agricultural production due to nematode infess tations are estimated at over 125 billion USD [1]. Parasitic nematodes belong to obligate endoparaa sites with a sedentary localization at places of host plant invasion. They begin their life cycle as nonfeedd ing organisms, but at the juvenile development stage they turn into infectious larvae that move from soil to the roots of host plants. For successful parasitism, nematodes use secretory proteins, introducing the latter through a tiny opening in injecting tubes (stylet) into metabolically active multinucleate specialized plant cells from which nemm atodes uptake nutrients [2]. These cells—feeding sites (syncytia)—are formed from ordinary plant cells in the process of cell differentiation and resemble either giant cells that are specific to root–knot nematodes or cysttresembling cells typical for cyst nematodes. Secretory proteins of nematodes induce dramatic host gene expression alterations in infected plant cells either through direct penetration into the nucleus [2, 3] or indirectly through intermediate proteins [4, 5], and, as a result, the cell cycle is alterated [6]; cytoskeleton is reorganized [7]; the processes of endoreduplication, target protein degradation [8], and the regulation of signaling and metabolic pathways [9] are disturbed; the phytohormone balance is altered [10]; a plant's protective immune responses are weakk ened; and its overall growth and development are suss pended [11].