Molecular Network for Regulation of Seed Size in Plants.

The size of seeds is particularly important for agricultural development, as it is a key trait that determines yield. It is controlled by the coordinated development of the integument, endosperm, and embryo. Large seeds are an important way of improving the ultimate "sink strength" of crops, providing more nutrients for early plant growth and showing certain tolerance to abiotic stresses. There are several pathways for regulating plant seed size, including the HAIKU (IKU) pathway, ubiquitin-proteasome pathway, G (Guanosine triphosphate) protein regulatory pathway, mitogen-activated protein kinase (MAPK) pathway, transcriptional regulators pathway, and phytohormone regulatory pathways including the auxin, brassinosteroid (BR), gibberellin (GA), jasmonic acid (JA), cytokinin (CK), Abscisic acid (ABA), and microRNA (miRNA) regulatory pathways. This article summarizes the seed size regulatory network and prospective ways of improving yield. We expect that it will provide a valuable reference to researchers in related fields.

Cytokinin regulates female gametophyte development by cell cycle modulation in Arabidopsis thaliana.

Male and female gametophyte development, double fertilization, and embryogenesis are key to alternating generations in angiosperms. The female gametophyte of Arabidopsis is an eight-nucleate haploid structure developed from functional megaspores (FMs) through three flawless mitoses regulated by a series of cell cycle genes. Cytokinin, an important phytohormone, plays a critical role in the regulation of plant growth and development. However, the mechanisms by which cytokinins regulate female gametophyte development remain largely unknown. In this study, we constructed transgenic plants (pES1::CKX1) with low cytokinin levels in the embryo sac. Phenotypic analysis showed that pES1::CKX1 inhibits female gametophyte development. Microscopic observation revealed that female gametophyte development of pES1::CKX1 was delayed. The promoters of all cell cycle genes were cloned and transformed into wild-type (WT). We crossed these transgenic plants of cell cycle genes expressed in ovules with pES1::CKX1 and compared the expression level of ß-glucuronidase (GUS) in pES1::CKX1 and WT. Many cell cycle-regulated genes were up or downregulated in pES1::CKX1 compared with WT, and the embryo sac development cell cycle in cycd2;1/+ cycd3;3 was defective. Our results demonstrated that cytokinin affects cell division in the female gametophyte by affecting the expression of cell cycle genes.

Smoking and Risk of Urolithiasis: Meta-Analysis of Observational Studies.

Background: Earlier studies have warned about the effects of smoking on urolithiasis. Some studies have deemed that smoking has a promoting effect on urolithiasis, whereas others have considered that no inevitable association exists between the two. Therefore, we conducted a meta-analysis to estimate whether smoking is associated with urolithiasis risk. Methods: To identify publications from related observational studies, we performed a search on PubMed, Web of Science, Embase, and the Cochrane Library databases from inception until October 1, 2021. According to the heterogeneity, random-effect model was used to calculate the odds ratios (ORs) and corresponding 95% confidence intervals (CIs). Results: Five articles were included in the meta-analysis, representing data for 20,402 subjects, of which 1,758 (8.62%) had urolithiasis as defined according to the criteria. Three articles are concerned with analysis between ex-smokers and non-smokers, in which a significant difference was observed (OR = 1.73, 95% CI: 1.48-2.01). Our comparison of current smokers with non-smokers in another meta-analysis of three articles revealed no significant difference between them (OR = 1.08, 95% CI: 0.94-1.23). Finally, we separated subjects into ever-smokers and never-smokers and found a significant difference between the two groups in the analysis of three articles (OR = 1.31, 95% CI: 1.17-1.47). Sensitivity analysis confirmed the stability of the current results. Conclusion: Combined evidence from observational studies demonstrates a significant relation between smoking and urolithiasis. The trend of elevated urolithiasis risk from smoking was found in ever-smokers vs. never-smokers.