## 1 Introduction  
Root-knot nematodes (RKN) (_Meloidogyne_ species) are obligate sedentary parasites that cause considerable damage to crops by developing into plant roots. The rice nematode _Meloidogyne graminicola_ is prevalent across Asian and Latin American paddy rice (_Oryza sativa_ L.) fields [1, 2], and was recently reported in Italy [3]. Severe infections result in stunted root systems, which ultimately result in poor growth and crop production with substantial yield losses. _M. graminicola_-infected rice plants have characteristic swollen and hooked galls at root tips. RKN establish a feeding site in galls by inducing the differentiation of host cells into hypertrophied, multinucleate and metabolically active cells, named giant cells. This feeding structure serves as a constant food source to the nematode, allowing its development into a reproductive female, and completing its life cycle inside the host root. In rice _O. sativa_ Nipponbare plants, giant cells are visible as soon as two days post-infection (dpi) and egg-laying females can be observed from 18 to 22 dpi [4]. A main feature of plant-parasitic nematodes is the presence of a protractible stylet that serves to withdraw nutrients from the giant cells as well as to release molecules, including virulence effectors, in the apoplast or directly into the host cells [5; 6]. Effectors are molecules secreted by pathogens into the plant tissues to facilitate infection, by reprogramming the host metabolism, or by preventing the execution of plant defense responses. Sedentary nematodes mainly release effectors produced in their esophageal glands, through their stylet into host tissues, although other secretory organs may play a role in the parasitic process [7]. Transcriptomic, proteomic and comparative genomic approaches identified large repertoires of effector gene families in plant-parasitic nematodes [8]. In the rice-_M. graminicola_-compatible interaction, nematode effectors were identified from comprehensive transcriptomic analyses of pre-parasitic J2s and rice infected tissues [9; 10], spanning from J2 penetration to development into young adult females (from 2 to 16 dpi) [10]. Over the past years, novel _M. graminicola_ effectors playing a role in nematode parasitism were functionally characterized, including pioneer genes [11; 12; 13], a C-type lectin [14], and a protein disulfide isomerase (PDI) [15]. Several RKN effectors characterized so far on tomato or _Arabidopsis thaliana_ are able to interact with host proteins and consequently can interfere with cellular processes within the plant cell or in the apoplast to facilitate nematode infection (for review [6]). In addition, some _M. graminicola_ effectors are able to suppress the induced hypersensitive response (HR) in _Nicotiana benthamiana_ transient expression assays or reactive oxygen species (ROS) production and may contribute to the protection of nematodes from oxidative damage. Effector proteins could play a role in suppressing host immunity to allow for successful infection of susceptible plants. However, we have only scarce knowledge about RKN genes that are involved in the infection of resistant hosts. Are there specific effectors produced in response to host defense reactions? Does the nematode adapt its gene expression to different host genotypes? Studies focusing on the secretome of _Meloidogyne incognita_ interacting with a resistant host genotype evidenced few changes in nematode gene expression, associated to degrading enzymes, antioxidant, autophagy and cytoskeleton-related processes [16; 17]. The aim of this study was to identify the nematode genes expressed in resistant plants and highlight the major changes occurring in their pattern of expression as compared to susceptible plants. In rice, genetic resistance to _M. graminicola_ has been found only in a few _O. sativa_ varieties [18; 19; 20] and in some rice relative species, including the African rice _Oryza glaberrima_[21; 22] and the South-American wild rice _Oryza glumapeatula_[23].