The shoot apical meristem (SAM), which is formed during embryogenesis, generates leaves, stems, and floral organs during the plant life cycle. SAM development is controlled by SHOOT MERISTEMLESS (STM), a conserved Class I KNOX transcription factor that interacts with another subclass homeodomain protein, BELL, to form a heterodimer, which regulates gene expression at the transcriptional level in Arabidopsis (Arabidopsis thaliana). Meanwhile, SKI-INTERACTING PROTEIN (SKIP), a conserved protein in eukaryotes, works as both a splicing factor and as a transcriptional regulator in plants to control gene expression at the transcriptional and posttranscriptional levels by interacting with distinct partners. Here, we show that, similar to plants with a loss of function of STM, a loss of function of SKIP or the specific knockout of SKIP in the SAM region resulted in failed SAM development and the inability of the mutants to complete their life cycle. In comparison, Arabidopsis mutants that expressed SKIP specifically in the SAM region formed a normal SAM and were able to generate a shoot system, including leaves and floral organs. Further analysis confirmed that SKIP interacts with STM in planta and that SKIP and STM regulate the expression of a similar set of genes by binding to their promoters. In addition, STM also interacts with EARLY FLOWERING 7 (ELF7), a component of Polymerase-Associated Factor 1 complex, and mutation in ELF7 exhibits similar SAM defects to that of STM and SKIP. This work identifies a component of the STM transcriptional complex and reveals the mechanism underlying SKIP-mediated SAM formation in Arabidopsis.

Fusarium ear rot (FER), caused by Fusarium verticillioides (F. verticillioides), is a major disease of maize that reduces grain yield and quality globally. However, few major loci for FER have been verified and cloned. Resistance to FER is a quantitative trait influenced by environmental conditions, and maize genotypes completely resistant to the pathogen remain unknown. To gain a comprehensive understanding of the genetic basis of natural variation in FER resistance, a recombinant inbred line (RIL) population consisting of 257 progenies was developed by crossing the resistant line BT with the susceptible line Xi502. This population was genotyped using a set of 6807 high-density single nucleotide polymorphism (SNP) markers developed in this study. As a result, a total of five QTLs were identified by linkage mapping across three years, located on five chromosomes, and explaining 4.38–13.13% of the phenotypic variation. Among these was a major QTL, qFER5-2. Located on chromosome 5 within the interval 185568562–185574073, qFER5-2 explained 13.13% of the total phenotypic variance. The two candidate genes within qFER5-2 exhibited distinct expression profiles between the BT and Xi502 inbred lines, suggesting their potential association with FER resistance. Collectively, these findings provide candidate genetic resources for further investigation and offer potentially useful materials for maize disease resistance breeding.

Visualization of cell structure with fluorescent dye for characterizing cell size, shape, and arrangement is a common method to study tissue morphology and morphogenesis. In order to observe shoot apical meristem (SAM) in Arabidopsis thaliana by laser scanning confocal microscopy, we modified the pseudo-Schiff propidium iodide staining method by adding a series solution treatment to stain the deep cells. The advantage of this method is mainly reflected by the direct observation of the clearly bounded cell arrangement and the typical three-layer cells in SAM without the traditional tissue slicing.