Flowering time variation in soybean is well characterized within domesticated germplasms and is critical for modern production, but its importance during domestication is unclear. Recently, Lu et al. (Nature Genetics, 2020) reported that two homeologous pseudo‐response‐regulator genes, Tof12 and Tof11, were sequentially selected in early soybean evolution for ancient flowering time adaptation and intensification of crop cultivation.

Rejuvenation refers to the process enabling plants to regain physiological and molecular characteristics lost after entering the adult phase. The underlying molecular mechanism is poorly understood. Previous studies have revealed that microRNA156 (miR156) is highly accumulated at juvenile stage and maintains juvenile traits by repressing a group of SQUAMOSA PROMOTER BINDING PROTEIN‐LIKE (SPL) transcription factors. Here, we found that induction of miR156 expression in adult leaves can only restore some aspects of juvenile traits, such as loss of epidermal leaf hairs on the lower side of leaves and absence of serration at the leaf edges, but is incapable of delaying flowering and promoting adventitious root production.

Arabidopsis thaliana CERK1 is an essential receptor‐like kinase in the chitin signal transduction pathway. The juxtamembrane (JM) domain of CERK1 regulates the kinase activity of this receptor. Here we demonstrate that the JM domains of LysM‐RLKs, CERK1, and OsCERK1 play a functionally conserved role in the activation of chitin signaling in Arabidopsis. The C‐termini of the JM domains of both CERK1 and OsCERK1 are indispensable for their function. Moreover, after replacing the JM domain of CERK1 with that of the nonhomologous RLK, BAK1 (CJBa) or FLS2 (CJFl), the chimeric CERK1 receptors maintained their ability to activate chitin signaling in Arabidopsis. Interestingly, the heterologous expression of CJBa and CJFl did not induce cell death in Nicotiana benthamiana leaves. These results suggest that the JM domains of CERK1, BAK1, and FLS2 play a conserved role in chitin signaling via a mechanism not related to sequence homology.

In eukaryotic cells, gene expression is greatly influenced by the dynamic chromatin environment. Epigenetic mechanisms, including covalent modifications to DNA and histone tails and the accessibility of chromatin, create various chromatin states for stress‐responsive gene expression that is important for adaptation to harsh environmental conditions. Recent studies have revealed that many epigenetic factors participate in abiotic stress responses, and various chromatin modifications are changed when plants are exposed to stressful environments. In this review, we summarize recent progress on the cross‐talk between abiotic stress response pathways and epigenetic regulatory pathways in plants. Our review focuses on epigenetic regulation of plant responses to extreme temperatures, drought, salinity, the stress hormone abscisic acid, nutrient limitations and ultraviolet stress, and on epigenetic mechanisms of stress memory.

Auxin is a crucial phytohormone, controlling multiple aspects of plant growth and responses to the changing environment. However, the role of local auxin biosynthesis in specific developmental programs remains unknown in crops. This study characterized the rice tillering and small grain 1 (tsg1) mutant, which has more tillers but a smaller panicle and grain size resulting from a reduction in endogenous auxin. TSG1 encodes a tryptophan aminotransferase that is allelic to the FISH BONE (FIB) gene. The tsg1 mutant showed hypersensitivity to indole‐3‐acetic acid and the competitive inhibitor of aminotransferase, L‐kynurenine. TSG1 knockout resulted in an increased tiller number but reduction in grain number and size, and decrease in height. Meanwhile, deletion of the TSG1 homologs OsTAR1, OsTARL1, and OsTARL2 caused no obvious changes, although the phenotype of the TSG1/OsTAR1 double mutant was intensified and infertile, suggesting gene redundancy in the rice tryptophan aminotransferase family. Interestingly, TSG1 and OsTAR1, but not OsTARL1 and OsTARL2, displayed marked aminotransferase activity. Meanwhile, subcellular localization was identified as the endoplasmic reticulum, while phylogenetic analysis revealed functional divergence of TSG1 and OsTAR1 from OsTARL1 and OsTARL2. These findings suggest that TSG1 dominates the tryptophan aminotransferase family, playing a prominent role in local auxin biosynthesis in rice.

Both phototropins (phot1 and phot2) and cryptochromes (cry1 and cry2) were proven as the Arabidopsis thaliana blue light receptors. Phototropins predominately function in photomovement, and cryptochromes play a role in photomorphogenesis. Although cryptochromes have been proposed to serve as positive modulators of phototropic responses, the underlying mechanism remains unknown. Here, we report that depleting sucrose from the medium or adding gibberellic acids (GAs) can partially restore the defects in phototropic curvature of the phot1 phot2 double mutants under high‐intensity blue light; this restoration does not occur in phot1 phot2 cry1 cry2 quadruple mutants and nph3 (nonphototropic hypocotyl 3) mutants which were impaired phototropic response in sucrose‐containing medium. These results indicate that GAs and sucrose antagonistically regulate hypocotyl phototropism in a cryptochromes dependent manner, but it showed a crosstalk with phototropin signaling on NPH3. Furthermore, cryptochromes activation by blue light inhibit GAs synthesis, thus stabilizing DELLAs to block hypocotyl growth, which result in the higher GAs content in the shade side than the lit side of hypocotyl to support the asymmetric growth of hypocotyl. Through modulation of the abundance of DELLAs by sucrose depletion or added GAs, it revealed that cryptochromes have a function in mediating phototropic curvature.

Iron (Fe) is indispensable for the growth and development of plants. It is well known that FER‐LIKE FE DEFICIENCY‐INDUCED TRANSCRIPTION FACTOR (FIT) is a key regulator of Fe uptake in Arabidopsis. Here, we identify the Oryza sativa FIT (also known as OsbHLH156) as the interacting partner of IRON‐RELATED BHLH TRANSCRIPTION FACTOR 2 (OsIRO2) that is critical for regulating Fe uptake. The OsIRO2 protein is localized in the cytoplasm and nucleus, but OsFIT facilitates the accumulation of OsIRO2 in the nucleus. Loss‐of‐function mutations of OsFIT result in decreased Fe accumulation, severe Fe‐deficiency symptoms, and disrupted expression of Fe‐uptake genes. In contrast, OsFIT overexpression promotes Fe accumulation and the expression of Fe‐uptake genes. Genetic analyses indicate that OsFIT and OsIRO2 function in the same genetic node. Further analyses suggest that OsFIT and OsIRO2 form a functional transcription activation complex to initiate the expression of Fe‐uptake genes. Our findings provide a mechanism understanding of how rice maintains Fe homeostasis.

MicroRNAs (miRNAs) play important roles in rice response to Magnaporthe oryzae, the causative agent of rice blast disease. Studying the roles of rice miRNAs is of great significance for the disease control. Osa‐miR167d belongs to a conserved miRNA family targeting auxin responsive factor (ARF) genes that act in developmental and stress‐induced responses. Here, we show that Osa‐miR167d plays a negative role in rice immunity against M. oryzae by suppressing its target gene. The expression of Osa‐miR167d was significantly suppressed in a resistant accession at and after 24 h post inoculation (hpi), however, its expression was significantly increased at 24 hpi in the susceptible accession upon M. oryzae infection. Transgenic rice lines over‐expressing Osa‐miR167d were highly susceptible to multiple blast fungal strains. By contrast, transgenic lines expressing a target mimicry to block Osa‐miR167d enhanced resistance to rice blast disease. In addition, knocking out the target gene ARF12 led to hyper‐susceptibility to multiple blast fungal strains. Taken together, our results indicate that Osa‐miR167d negatively regulate rice immunity to facilitate the infection of M. oryzae by downregulating ARF12. Thus, Osa‐miR167d‐ARF12 regulatory module could be valuable in improvement of blast‐disease resistance.