Increasing crop yields can provide food, animal feed, bioenergy feedstocks and biomaterials to meet increasing global demand; however, the methods used to increase yield can negatively affect sustainability. For example, application of excess fertilizer can generate and maintain high yields but also increases input costs and contributes to environmental damage through eutrophication, soil acidification and air pollution. Improving crop nutrient efficiency can improve agricultural sustainability by increasing yield while decreasing input costs and harmful environmental effects. Here, we review the mechanisms of nutrient efficiency (primarily for nitrogen, phosphorus, potassium and iron) and breeding strategies for improving this trait, along with the role of regulation of gene expression in enhancing crop nutrient efficiency to increase yields. We focus on the importance of root system architecture to improve nutrient acquisition efficiency, as well as the contributions of mineral translocation, remobilization and metabolic efficiency to nutrient utilization efficiency.

Plant species exhibit substantial variation in leaf morphology. We isolated a recessive mutant gene termed small and cordate leaf 1 (scl1) that causes alteration in both leaf size and shape of cucumber. Compared to wild type leaves, the scl1 mutant had fewer numbers of epidermal pavement cells. A single nucleotide polymorphism was associated with this leaf phenotype, which occurred in a putative nucleoside bisphosphate phosphatase. RNA-seq analysis of the wild type and scl1 mutant leaves suggested that SCL1 regulation may not involve known hormonal pathways. Our work identified a candidate gene for SCL1 that may play a role in leaf development.

Dedifferentiation is a remarkable process that produces pluripotent stem cells from differentiated somatic cells to ensure developmental plasticity. Plants have evolved the ability of cellular dedifferentiation, and signaling cascades related to auxin and cytokinin-dependent callus formation have been extensively investigated. However, the molecular mechanism underlying sugar-dependent callus formation remains unknown. Here, we show that sugar-dependent callus formation is mainly regulated by the TOR-E2Fa module in Arabidopsis. Sugar-activated TOR kinase phosphorylates and stabilizes E2Fa proteins to transcriptionally activate S-phase genes during callus formation. In parallel, E2Fa is transcriptionally regulated by the ARF-LBD transcription cascade. Multi-layered regulation of E2Fa by sugar and auxin is likely to shape balanced cellular dedifferentiation capability in Arabidopsis.

Auxin and cytokinin direct cell proliferation and differentiation during the in vitro culture of plant cells, but the molecular basis of these processes, especially de novo shoot regeneration, has not been fully elucidated. Here, we describe the regulatory control of shoot regeneration in Arabidopsis thaliana (L.) Heynh, based on the interaction of ARABIDOPSIS RESPONSE REGULATOR12 (ARR12) and WUSCHEL (WUS). The major site of ARR12 expression coincided with the location where the shoot apical meristem (SAM) initiated. The arr12 mutants showed severely impaired shoot regeneration and reduced responsiveness to cytokinin; consistent with this, the overexpression of ARR12 enhanced shoot regeneration. Certain shoot meristem specification genes, notably WUSCHEL (WUS) and CLAVATA3, were significantly downregulated in the arr12 explants. Chromatin immunoprecipitation (ChIP) and transient activation assays demonstrated that ARR12 binds to the promoter of WUS. These observations indicate that during shoot regeneration, in vitro, ARR12 functions as a molecular link between cytokinin signaling and the expression of shoot meristem specification genes.