Photosynthesis is a universal process for plant survival, and immune defense is also a key process in adapting to the growth environment. Various studies have indicated that these two processes are interconnected in a complex network. Photosynthesis can influence signaling pathways and provide both materials and energy for immune defense, while the immune defense process can also have feedback effects on photosynthesis. Pathogen infection inevitably leads to changes in photosynthesis parameters, including Pn, Gs, and Ci; biochemical materials such as SOD and CAT; signaling molecules such as H₂O₂ and hormones; and the expression of genes involved in photosynthesis. Some researchers have found that changes in photosynthesis activity are related to the resistance level of the host, the duration after infection, and the infection position (photosynthetic source or sink). Interactions between wheat and the main fungal pathogens, such as Puccinia striiformis, Blumeria graminis, and Fusarium graminearum, constitute an ideal study system to elucidate the relationship between changes in host photosynthesis and resistance levels, based on the accessibility of methods for artificially controlling infection and detecting changes in photosynthesis, the presence of multiple pathogens infecting different positions, and the abundance of host materials with various resistance levels. This review is written only from the perspective of plant pathologists, and after providing an overview of the available data, we generally found that changes in photosynthesis in the early stage of pathogen infection could be a causal factor influencing acquired resistance, while those in the late stage could be the result of resistance formation.

CN17 is a functional stay‐green wheat variety that exhibits delayed leaf senescence and enhanced photosynthetic competence. To better understand these valuable traits, levels of chlorophyllaandb, soluble proteins, unsaturated fatty acids, and other components of CN17 were assayed. In addition, chloroplast ultrastructure, chloroplast number, and differences in gene expression between CN17 and a control variety, MY11, were examined. By 21 d post‐anthesis (DPA), CN17 leaves exhibited a significantly higher maximal photochemical efficiency for photosystem II (PSII) (F_v/F_m) and a significantly higher efficiency of excitation capture by open PSII reaction centres (F_v′/F_m′). In addition, chlorophyll degradation in CN17 was delayed by approximately 14 d, and was not blocked as observed in cosmetic stay‐green phenotypes. The soluble protein content (Ps) of CN17 was higher than MY11 at all timepoints assayed, and the ratio of unsaturated to saturated fatty acids was significantly higher. CN17 also exhibited isolated granal lamellae associated with vesicles and diminished peroxidation, and between 35 and 42 DPA, a sharp decrease in chloroplast number was detected. Taken together, these results strongly support the hypothesis that chloroplast ultrastructure regeneration is responsible for the functional stay‐green trait of CN17, and gene expression data provide insight into the mechanistic details.

Photosynthesis is not only a primary generator of reactive oxygen species (ROS) but also a component of plant defence. To determine the relationships among photosynthesis, ROS, and defence responses to powdery mildew in wheat, we compared the responses of the Pm40-expressing wheat line L658 and its susceptible sister line L958 at 0, 6, 12, 24, 48, and 72 h post-inoculation (hpi) with powdery mildew via analyses of transcriptomes, cytology, antioxidant activities, photosynthesis, and chlorophyll fluorescence parameters. The results showed that H₂O₂ accumulation in L658 was significantly greater than that in L958 at 6 and 48 hpi, and the enzymes activity and transcripts expression of peroxidase and catalase were suppressed in L658 compared with L958. In addition, the inhibition of photosynthesis in L658 paralleled the global downregulation of photosynthesis-related genes. Furthermore, the expression of the salicylic acid-related genes non-expressor of pathogenesis related genes 1 (NPR1), pathogenesis-related 1 (PR1), and pathogenesis-related 5 (PR5) was upregulated, while the expression of jasmonic acid- and ethylene-related genes was inhibited in L658 compared with L958. In conclusion, the downregulation of photosynthesis-related genes likely led to a decline in photosynthesis, which may be combined with the inhibition of peroxidase (POD) and catalase (CAT) to generate two stages of H₂O₂ accumulation. The high level of H₂O_2, salicylic acid and PR1 and PR5 in L658 possible initiated the hypersensitive response.

Stripe rust, a highly destructive foliar disease of wheat (Triticum aestivum), causes severe losses, which may be accompanied by reduced photosynthetic activity and accelerated leaf senescence. We used suppression subtractive hybridization (SSH) to examine the mechanisms of resistance in the resistant wheat line L693 (Reg. No. GP-972, PI 672538), which was derived from a lineage that includes a wide cross between common and Thinopyrum intermedium. Sequencing of an SSH cDNA library identified 112 expressed sequence tags. In silico mapping placed one of these tags [GenBank: JK972238] on chromosome 1A. Primers based on [GenBank: JK972238] amplified a polymorphic band, which co-segregated with YrL693. We cloned a candidate gene encoding wheat copper-binding protein (WCBP1) by amplifying the polymorphic region, and we mapped WCBP1 to a 0.64 cM genetic interval. Brachypodium, rice, and sorghum have genes and genomic regions syntenic to this region. Sequence analysis suggested that the resistant WCBP1 allele might have resulted from a deletion of 36-bp sequence of the wheat genomic sequence, rather than direct transfer from Th. intermedium. qRT-PCR confirmed that WCBP1 expression changes in response to pathogen infection. The unique chromosomal location and expression mode of WCBP1 suggested that WCBP1 is the putative candidate gene of YrL693, which was involved in leaf senescence and photosynthesis related to plant responses to stripe rust infection during the grain-filling stage.