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Ramie fiber extracted from ramie stem bark (RSB) is a highly important natural fiber, and therefore, RSB is an economically important plant organ. The genetic basis of RSB traits is poorly understood. In the present study, fiber yield and three RSB traits (bark thickness, bark weight, and fiber output ratio) were subject to quantitative trait locus (QTL) analysis using an F2 agamous line population derived from two ramie varieties (Qingdaye and Zhongzhu 1). A total of 4338 high-quality single nucleotide polymorphisms were identified using the genotyping-by-sequencing technique and were subsequently used to construct a high-density genetic map spanning 1942.9 cM. Thereafter, QTL analysis identified five, two, four, and four QTLs for bark thickness, bark weight, fiber output ratio, and fiber yield, respectively. A 5.1 cM region that corresponded to a QTL for bark thickness (qBT4a) contained 106 candidate genes, and the Zhongzhu 1 allele of one of the genes, a putative MYB gene (evm.model.scaffold7373.133_D1), included a 760-bp insertion that caused premature termination, thereby producing a protein that lacked part of the MYB domain. Because MYB transcription factors play central roles in regulating the development of secondary cellular walls and fiber biosynthesis, we propose evm.model.scaffold7373.133_D1 as a likely candidate gene for qBT4a.

The RNA binding protein Celf1 regulates alternative splicing in the nucleus and mRNA stability and translation in the cytoplasm. Celf1 is strongly down-regulated during mouse postnatal heart development. Its re-induction in adults induced severe heart failure and reversion to fetal splicing and gene expression patterns. However, the impact of Celf1 depletion on cardiac transcriptional and posttranscriptional dynamics in neonates has not been addressed. We found that homozygous Celf1 knock-out neonates exhibited cardiac dysfunction not observed in older homozygous animals, although homozygous mice are smaller than wild type littermates throughout development. RNA-sequencing of mRNA from homozygous neonatal hearts identified a network of cell cycle genes significantly up-regulated and down-regulation of ion transport and circadian genes. Cell cycle genes are enriched for Celf1 binding sites supporting a regulatory role in mRNA stability of these transcripts. We also identified a cardiac splicing network coordinated by Celf1 depletion. Target events contain multiple Celf1 binding sites and enrichment in GU-rich motifs. Identification of direct Celf1 targets will advance our knowledge in the mechanisms behind developmental networks regulated by Celf1 and diseases where Celf1 is mis-regulated.