A novel yellow-green leaf mutant yellow-green leaf-1 (ygl-1) was isolated in self-pollinated progenies from the cross of maize inbred lines Ye478 and Yuanwu02. The mutant spontaneously showed yellow-green character throughout the lifespan. Meanwhile, the mutant reduced contents of chlorophyll and Car, arrested chloroplast development and lowered the capacity of photosynthesis compared with the wild-type Lx7226. Genetic analysis revealed that the mutant phenotype was controlled by a recessive nuclear gene. The ygl-1 locus was initially mapped to an interval of about 0.86 Mb in bin 1.01 on the short arm of chromosome 1 using 231 yellow-green leaf individuals of an F2 segregating population from ygl-1/Lx7226. Utilizing four new polymorphic SSR markers, the ygl-1 locus was narrowed down to a region of about 48 kb using 2930 and 2247 individuals of F2 and F3 mapping populations, respectively. Among the three predicted genes annotated within this 48 kb region, GRMZM2G007441, which was predicted to encode a cpSRP43 protein, had a 1-bp nucleotide deletion in the coding region of ygl-1 resulting in a frame shift mutation. Semi-quantitative RT-PCR analysis revealed that YGL-1 was constitutively expressed in all tested tissues and its expression level was not significantly affected in the ygl-1 mutant from early to mature stages, while light intensity regulated its expression both in the ygl-1 mutant and wild type seedlings. Furthermore, the mRNA levels of some genes involved in chloroplast development were affected in the six-week old ygl-1 plants. These findings suggested that YGL-1 plays an important role in chloroplast development of maize.

Inbreeding depression is widespread across plant and animal kingdoms and may arise from the exposure of deleterious alleles and/or loss of overdominant alleles resulting from increased homozygosity, but these genetic models cannot fully explain the phenomenon. Here, we report epigenetic links to inbreeding depression in maize. Teosinte branched1/cycloidea/proliferating cell factor (TCP) transcription factors control plant development. During successive inbreeding among inbred lines, thousands of genomic regions across TCP-binding sites (TBS) are hypermethylated through the H3K9me2-mediated pathway. These hypermethylated regions are accompanied by decreased chromatin accessibility, increased levels of the repressive histone marks H3K27me2 and H3K27me3, and reduced binding affinity of maize TCP-proteins to TBS. Consequently, hundreds of TCP-target genes involved in mitochondrion, chloroplast, and ribosome functions are down-regulated, leading to reduced growth vigor. Conversely, random mating can reverse corresponding hypermethylation sites and TCP-target gene expression, restoring growth vigor. These results support a unique role of reversible epigenetic modifications in inbreeding depression.

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Leucine-rich repeat (LRR)-receptor-like protein kinases (LRR-RLKs) play vital roles in plant growth, development, and responses to environmental stresses. In this study, a new LRR-RLK gene, ZmRLK7 , was isolated from maize, and its function within plant development was investigated through ectopic expression in Arabidopsis . The spatial expression pattern analysis reveals that ZmRLK7 is highly expressed in embryos prior to programmed cell death (PCD) of starchy endosperm tissues, and its encoded protein has been localized to both plasm and nuclear membranes subcellularly. Overexpression of sense ZmRLK7 reduced the plant height, organ size (e.g., petals, silique, and seeds), and 1000-seed weight in transgenic lines, while the antisense transgene enlarged these traits. Cytological analysis suggested that ZmRLK7 negatively regulates petal size through restricting both cell expansion and proliferation. In addition, abnormal epidermal cell structure was observed, and the stomata number decreased obviously in sense ZmRLK7 transgenic lines with a lower stomatal index than that in the wild type. Quantitative RT-PCR analysis indicated that transcript levels of genes that are involved in the brassinosteroid and ERACTA signaling pathways were coordinately altered, which could partially explain the phenotypic variation. Moreover, overexpression of antisense ZmRLK7 substantially rescued the Arabidopsis bak1-3 mutant phenotype. All these results together suggest that ZmRLK7 can serve as an important regulator in regulating plant architecture and organ size formation. This work will provide insight into the function of ZmRLK7 in maize.

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