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Background: Sleep disorders are a significant health issue that urgently needs to be addressed among undergraduate students, and one of the potential underlying problems could be problematic smartphone use (PSU). This study aimed to clarify the relationship between PSU and poor sleep quality by investigating the independent and serial mediating roles of anxiety and depressive symptoms in a population of university students in Tibet, China. Methods: A total of 2993 Tibetan college students completed three waves of data surveys, with all participants completing questionnaires on PSU, anxiety, depressive symptoms, and sleep quality (Time 1 (T1) -Time 3 (T3)). Bootstrapped mediation analysis was used to explore the mediating role of anxiety and depressive symptoms in the longitudinal relationship between PSU and sleep quality. Results: Both direct and indirect effects of PSU on poor sleep quality were found. PSU (T1) can had not only a direct negative influence on poor sleep quality (T3) among young adults (direct effect = 0.021, 95% CI = 0.010-0.033) but also an indirect negative impact via three pathways: the independent mediating effect of anxiety symptoms (T2) (indirect effect 1 = 0.003, 95% CI = 0.001-0.006), the independent mediating effect of depressive symptoms (T2) (indirect effect 2 = 0.004, 95% CI = 0.002-0.006), and the serial mediating effects of anxiety (T2) and depressive symptoms (T2) (indirect effect 3 = 0.008, 95% CI=0.005-0.011). Conclusion: These findings highlight the role of anxiety and depression symptoms as joint mediating factors in the relationship between PSU and sleep disturbances. Interventions focused on improving sleep that incorporate behavioural measures could benefit from treatment approaches targeting mental disorders.
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Heterosis refers to the better performance of cross progeny compared with inbred parents, and its utilization contributes greatly to agricultural production. Several hypotheses have been proposed to explain heterosis mainly including dominance, over-dominance (or pseudo-overdominance) and epistasis. However, systematic dissection and verification of these hypotheses are rarely documented. Here, comparison of heterosis level across different traits showed that the strong heterosis of composite traits (such as yield) could be attributed to the multiplicative effects of moderate heterosis of component traits, whether at the genome or locus level. Yield heterosis was regulated by a complex trait-QTL network that was characterized by obvious centre-periphery structure, hub QTL, complex up/downstream and positive/negative feedback relationships. More importantly, we showed that better-parent heterosis on yield could be produced in a cross of two near-isogenic lines by the pyramiding and complementation of two major heterotic QTL showing partial-dominance on yield components. The causal gene (BnaA9.CYP78A9) of QC14 was identified, and its heterotic effect results from the heterozygous status of a CACTA-like transposable element in its upstream regulatory region, which led to partial dominance at expression and auxin levels, thus resulting in non-additive expression of downstream responsive genes involved in cell cycle and proliferation, eventually leading to the heterosis of cell number. Taken together, the results at the phenotypic, genetic and molecular levels were highly consistent, which demonstrated that the pyramiding effect of heterotic QTL and the multiplicative effect of individual component traits could well explain substantial parts of yield heterosis in oilseed rape. These results provide in-depth insights into the genetic architecture and molecular mechanism of yield heterosis.
Assuntos
Vigor Híbrido , Locos de Características Quantitativas , Vigor Híbrido/genética , Mapeamento Cromossômico , Locos de Características Quantitativas/genética , Fenótipo , HeterozigotoRESUMO
Seed size/weight is one of the key traits related to plant domestication and crop improvement. In rapeseed (Brassica napus L.) germplasm, seed weight shows extensive variation, but its regulatory mechanism is poorly understood. To identify the key mechanism of seed weight regulation, a systematic comparative study was performed. Genetic, morphological and cytological evidence showed that seed weight was controlled by maternal genotype, through the regulation of seed size mainly via cell number. The physiological evidence indicated that differences in the pod length might result in differences in pod wall photosynthetic area, carbohydrates and the final seed weight. We also identified two pleiotropic major quantitative trait loci that acted indirectly on seed weight via their effects on pod length. RNA-seq results showed that genes related to pod development and hormones were significantly differentially expressed in the pod wall; genes related to development, cell division, nutrient reservoir and ribosomal proteins were all up-regulated in the seeds of the large-seed pool. Finally, we proposed a potential seed weight regulatory mechanism that is specific to rapeseed and novel in plants. The results demonstrate a causal link between the size of the pod (mother, source) and the seed (offspring, sink) in rapeseed, which provides novel insight into the maternal control of seed weight and will open a new research field in plants.