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Poly(vinylidene fluoride) (PVDF)‐based polymers demonstrate great potential for applications in flexible and wearable electronics but show low piezoelectric coefficients (e.g., −d₃₃< 30 pC N⁻¹). The effective improvement for the piezoelectricity of PVDF is achieved by manipulating its semicrystalline structures. However, there is still a debate about which component is the primary contributor to piezoelectricity. Therefore, current methods to improve the piezoelectricity of PVDF can be classified into modulations of the amorphous phase, the crystalline region, and the crystalline–amorphous interface. Here, the basic principles and measurements of piezoelectric coefficients for soft polymers are first discussed. Then, three different categories of structural modulations are reviewed. In each category, the physical understanding and strategies to improve the piezoelectric performance of PVDF are discussed. In particular, the crucial role of the oriented amorphous fraction at the crystalline–amorphous interface in determining the piezoelectricity of PVDF is emphasized. At last, the future development of high performance piezoelectric polymers is outlooked.

 

Arabidopsis RESISTANCE TO POWDERY MILDEW 8.2 (RPW8.2) is specifically induced by the powdery mildew (PM) fungus (Golovinomyces cichoracearum) in the infected epidermal cells to activate immunity. However, the mechanism of RPW8.2-induction is not well understood. Here, we identify a G. cichoracearum effector that interacts with RPW8.2, named Gc-RPW8.2 interacting protein 1 (GcR8IP1), by a yeast two-hybrid screen of an Arabidopsis cDNA library. GcR8IP1 physically associated with RPW8.2 with its RING finger domain that is essential and sufficient for the association. GcR8IP1 was secreted and translocated into the nucleus of host cell infected with PM. Association of GcR8IP1 with RPW8.2 led to an increase of RPW8.2 in the nucleus. In turn, the nucleus-localised RPW8.2 promoted the activity of the RPW8.2 promoter, resulting in transcriptional self-amplification of RPW8.2 to boost immunity at infection sites. Additionally, ectopic expression or host-induced gene silencing of GcR8IP1 supported its role as a virulence factor in PM. Altogether, our results reveal a mechanism of RPW8.2-dependent defense strengthening via altered partitioning of RPW8.2 and transcriptional self-amplification triggered by a PM fungal effector, which exemplifies an atypical form of effector-triggered immunity.