OsAP79 is involved in BPH resistance by regulating the sclerenchyma layer thickness
The cell wall is an important barrier to disease and insect infestation. The gene Bph30 is strongly expressed in sclerenchyma cells, and enhances cellulose and hemicellulose syntheses, thereby creating stiffer cell walls and thicker sclerenchyma, which prevent BPH stylets from reaching the phloem (Shi et al ., 2021). A thicker sclerenchyma layer was also observed in the OE lines, indicating that OsAP79probably conferred resistance to BPH through fortified sclerenchyma layer (Figure 5). To explore the reasons, lignin deposition can contribute to thickening of sclerenchyma layer. For example, secondary cell wall thickness in fiber cells was reduced significantly through the positive regulation of lignin deposition by MYB85 involved in phenylpropane pathway (Zhong et al., 2008). Moreover, it is known that the precursors of lignin biosynthesis mainly originated from phenylalanine which derived from shikimic acid pathway (Wang et al., 2012; Tao et al., 2021). Consistently, metabolite analysis indicated that the content of shikimic acid significantly decreased in the OE and NIP lines after BPH infestation, but L-phenylalanine significant increased (Figure 6a). In addition, auxin transport also have a role in cell wall thickening. For instance, Arabidopsis thaliana treated with auxin transport inhibitor NPA resulted in the accumulation of IAA, which significantly repressed the secondary cell wall thickening (Lee et al., 2019). The present study indicated that OE lines of OsAP79decreased IAA content and fortified sclerenchyma layer (Figure 4f and 5). Therefore, we reasoned that the resistance conferred byOsAP79 involving fortifying the sclerenchyma may be associated with lignin deposition and auxin transport. Further research will be needed to clarify the specific mechanism.