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Yellowhorn ( Bunge) has been widely planted for biodiesel production in China, but has frequently shown poor field performance. Container-grown yellowhorn seedlings originating from three Chinese provenances, Wengniute Qi (WQ), Alukeerqin Qi (AQ), and Shanxian (SX), were fertilized with slow-release fertilizer (SRF) at 40, 80, 120, 160 or 200 mg N seedling. Tree growth, survival and nutrient content were measured after one yearâs growth in a greenhouse followed by two years in a field site. Plants from AQ and SX tended to have higher stem and root P contents in the nursery. Higher rates of SRF increased root N, and stem and root P contents. After one year in the nursery, there were a number of interactions between provenance and SRF for plant growth responses and nutrient content in the nursery, however after two years of additional growth in the field, plants from the different provenances generally responded similarly to applied SRF in the nursery, with few interactions. Final plant height was approximately 10% lower in trees from provenance SX but was not affected by application of SRF. Conversely, final trunk diameter and stem and root biomass were unaffected by provenance but increased with higher rates of applied SRF. Our results indicate that application of SRF may be a useful tool to nutrient load yellowhorn in the nursery and facilitate transplanting performance in the field. Overall, optimal nursery and field performance of yellowhorn were observed in provenance AQ at 120â200 mg N seedling SRF. We suggest that growers consider a wider range of yellowhorn provenances and SRF rates (above 200 mg N seedling) to yield even better growth response.Xanthoceras sorbifoliumâ1â1â1

Background: Mitochondrial dysfunction plays a crucial role in Type 2 Diabetes Mellitus (T2DM) and its complications. However, the genetic pathophysiology remains under investigation. Through multi-omics Mendelian Randomization (MR) and colocalization analyses, we identified mitochondrial-related genes causally linked with T2DM and its complications., Methods: Summary-level quantitative trait loci data at methylation, RNA, and protein levels were retrieved from European cohort studies. GWAS summary statistics for T2DM and its complications were collected from the DIAGRAM and FinnGen consortiums, respectively. Summary-data-based MR was utilized to estimate the causal effects. The heterogeneity in dependent instrument test assessed horizontal pleiotropy, while colocalization analysis determined whether genes and diseases share the same causal variant. Enrichment analysis, drug target analysis, and phenome-wide MR were conducted to further explore the biological functions, potential drugs, and causal associations with other diseases., Results: Integrating evidence from multi-omics, we identified 18 causal mitochondrial-related genes. Enrichment analysis revealed they were not only related to nutrient metabolisms but also to the processes like mitophagy, autophagy, and apoptosis. Among these genes, Tu translation elongation factor mitochondrial ( TUFM ), 3-hydroxyisobutyryl-CoA hydrolase ( HIBCH ), and iron-sulfur cluster assembly 2 ( ISCA2 ) were identified as Tier 1 genes, showing causal links with T2DM and strong colocalization evidence. TUFM and ISCA2 were causally associated with an increased risk of T2DM, while HIBCH showed an inverse causal relationship. The causal associations and colocalization effects for TUFM and HIBCH were validated in specific tissues. TUFM was also found to be a risk factor for microvascular complications in T2DM patients including retinopathy, nephropathy, and neuropathy. Furthermore, drug target analysis and phenome-wide MR underscored their significance as potential therapeutic targets., Conclusions: This study identified 18 mitochondrial-related genes causally associated with T2DM at multi-omics levels, enhancing the understanding of mitochondrial dysfunction in T2DM and its complications. TUFM , HIBCH , and ISCA2 emerge as potential therapeutic targets for T2DM and its complications., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Li, Miao, Feng, Zhu, Chen, Kang, Wang, Lu and Zhang.)