On the cover: Pathogens and their hosts are engaged in an ever-evolving arms race. Host pattern-recognition receptors detect invading fungi and recruit adaptor proteins to initiate a signaling cascade that ultimately triggers immune responses. In maize, the plasma-membrane-localized receptor ZmWAK recognizes an unknown signature from the fungal pathogen Sporisorium reilianum and relays the phosphorylation signal to the cytoplastic kinase ZmSnRK1α2, thereby facilitating its translocation into the nucleus for promoting the degradation of ZmWRKY53. The reduced accumulation of ZmWRKY53, in turn, causes the downregulated expression of transmembrane transporter genes, thereby restricting nutrient acquisition by Sporisorium reilianum in the apoplasts. Therefore, the ZmWAK-SnRK1α2-WRKY53 signaling module underlies quantitative resistance to head smut disease in maize. The cover portrays this host-pathogen conflict with a personified depiction, showing the soldiers in battle defending their supplies with a strategic counterattack against the enemies. Image by Mingzhu Yan.
MP:山东农大揭示光受体介导的耐密植新机制
密植会触发避荫反应从而影响植物生长发育。本研究发现玉米的密植效应（包括叶角和茎伸长效应）依赖于光受体 phytochrome B (phyB1/B2)。
phyB在蛋白水平上与IGULELESS1 (LG1)（ a classical key regulator of leaf angle）来影响植物生长构型及对密植的耐受性。LG1 的丰度在high R:FR light (low density)条件下受到phyB的正调控，但是在 low R:FR light (high density)条件下的丰度迅速下降，这直接影响了叶角和植物高度。
此外，作者还发现homeobox transcription factor HB53 被phyB and LG1抑制，但是在密植条件下被迅速诱导。HB53通过调控细胞分裂和伸长来影响密植条件下的植物构型。
小结：本研究揭示了光受体phyB介导的玉米耐密植新机制。
A proposed working model shows how the phyB-LG1-HB53 module regulates maize plant architecture in response to different plant densities.phyB-Pr, inactive form of phyB; phyB-Pfr, active form of phyB; LBS, LG1 binding sites; HBS, HB53 binding sites; SAR, shade avoidance response; HDT, high-density tolerance. Question marks indicate the unknown factors promoting the expression of HB53 and CYCs.
原文：Phytochrome B interacts with LIGULELESS1 to control plant architecture and density tolerance in maize
