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.