pathway [15; 16]. Enzymes in the L-galactose pathway consist of phosphoglucose isomerase (PGI), phosphomannose isomerase (PMI), phosphomannose mutase (PMM), GDP-mannnose pyrophosphrolase (GMP or VTC1), GDP-mannnose-3\({}^{\prime}\),5\({}^{\prime}\)-epimerase (GME), GDP-L-galactose phosphorylase (GGP or VTC2), L-galactose-1-phosphate phosphatase (GPP or VTC4), L-galactose dehydrogenase (GDH), and L-galactono-1,4-lactone dehydrogenase (GLDH). However, VTC1 catalyzes the formation of GDP-D-mannnose, which serves as a precursor for AsA synthesis and is critical for cell wall polysaccharide and glycoprotein synthesis [17]. There are three _OsVTC1_ homologous genes in the rice genome: _OsVTC1-1_, _OsVTC1-3_, and _OsVTC1-8_. AsA content is increased in _OsVTC1-1_ and _OsVTC1-3_ overexpression lines and not _OsVTC1-8_ overexpression lines, indicating that _OsVTC1-1_ and _OsVTC1-3_ are involved in plant AsA synthesis. _OsVTC1-1_ and _OsVTC1-3_ are involved in the production of AsA in rice leaves and roots, respectively [18]. Several studies have investigated the function of _VTC1_ gene in plants. Down-regulation of _OsVTC1-1_ genes led to increased superoxide (O\({}_{2}^{-}\)) anion and malondialdehydedehyde (MDA) levels as well as decreased chlorophyll levels as a result of decreased salt tolerance [19]. A previous study also showed that the overexpression of tomato _GMPase (VTC1)_ increased the AsA content in tobacco and led to increased thermal tolerance [20]. [PERSON] et al. [21] reported that bacterial and fungal hyphal development was suppressed in _vtc1 Arabidopsis_ mutants with lower levels of AsA. Similarly, the presence of dead cells and an increased resistance to _Pseudomonas syringae_ infection in _Arabidopsis_ were observed in _vtc1_ mutants [22]. These studies indicate that _VTC1_ is vital in plant responses to abiotic and biotic stresses. Many biological processes are altered after pathogen infection [23]. Upon infection with a biotrophic fungal pathogen, plants lose their ability to photosynthesize and mobilize nutrients [24]. Cell walls, as a physical barrier, are the first plant defense mechanism against pathogens. Upon infection, plants accumulate reinforcing polymers, such as callose and phenolic compounds, for cell wall strengthening [25; 26]. High sugar content in plant tissues is associated with plant resistance, serving as substrates for cell wall polymers, signaling molecules, and energy for defense responses [27; 28]. Furthermore, ROS accumulation in the plant's subcellular compartments, which is toxic to the cells, acts as signaling molecules during defense responses [29]. A previous study reported that ROS accumulation and cell death were observed in resistant accessions after infection with _Alternaria brassicae_ in _Arabidopsis_[30]. ROS also promote lipid peroxidation, detectable by measuring malondialdehydedehyde (MDA) content [31]. In incompatible rice and _M. oryzae_ interactions, ROS accumulation and increased MDA content were measured, which ultimately resulted in HR cell death [32]. Additionally, plant hormones are pivotal in regulating plant defense against various pathogens [33]. Among several plant hormones, salicylic acid (SA) and jasmonic acid (JA) are key in defense against insect herbivores and microbial pathogens [34]. Although, the above studies revealed that pathogen infections induce several defense mechanisms in plants, it remains unclear how AsA synthesis is affected during rice defense responses. _OsVTC1-1_ in the AsA synthesis pathway might affect defenses against rice blast infections through several processes. Therefore, the aim of the present study was to investigate the role of _OsVTC1-1_ during rice blast infection. We compared cell wall monosaccharide composition, photosynthetic efficiency, AsA content, superoxide anion (O\({}_{2}^{-}\)) levels, malondialdehydedehyde (MDA) content, transcriptome, and proteome between wild type (WT) and _OsVTC1-1_ RNAi lines after rice blast fungus infection.