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Gene duplications have long been recognized as a driving force in the evolution of genes, giving rise to novel functions. The soybean (Glycine max) genome is characterized by a large number of duplicated genes. However, the extent and mechanisms of functional divergence among these duplicated genes in soybean remain poorly understood. In this study, we revealed that 4 MYB genes (GmMYBA5, GmMYBA2, GmMYBA1, and Glyma.09g235000)—presumably generated by tandem duplication specifically in the Phaseoleae lineage—exhibited a stronger purifying selection in soybean compared to common bean (Phaseolus vulgaris). To gain insights into the diverse functions of these tandemly duplicated MYB genes in anthocyanin biosynthesis, we examined the expression, transcriptional activity, induced metabolites, and evolutionary history of these 4 MYB genes. Our data revealed that Glyma.09g235000 is a pseudogene, while the remaining 3 MYB genes exhibit strong transcriptional activation activity, promoting anthocyanin biosynthesis in different soybean tissues. GmMYBA5, GmMYBA2, and GmMYBA1 induced anthocyanin accumulation by upregulating the expression of anthocyanin pathway-related genes. Notably, GmMYBA5 showed a lower capacity for gene induction compared to GmMYBA2 and GmMYBA1. Metabolomics analysis further demonstrated that GmMYBA5 induced distinct anthocyanin accumulation in Nicotiana benthamiana leaves and soybean hairy roots compared to GmMYBA2 and GmMYBA1, suggesting their functional divergence leading to the accumulation of different metabolites accumulation following gene duplication. Together, our data provide evidence of functional divergence within the MYB gene cluster following tandem duplication, which sheds light on the potential evolutionary directions of gene duplications during legume evolution. Tandemly duplicated MYB genes in regulation of anthocyanin biosynthesis exhibit functional divergence and a strong purifying selection in soybean. [ABSTRACT FROM AUTHOR]

Context Gestational diabetes mellitus (GDM) is a risk factor for child neurodevelopmental delay. Maternal short sleep duration (SSD) may aggravate glucose metabolism disorder in women with GDM. However, it is unclear whether maternal SSD will further affect the neurodevelopmental outcomes of children. Objective To identify the association of GDM complicated with SSD and child neurodevelopmental delay. Methods This prospective study included 7069 mother-child pairs. Between 24 and 28 weeks of gestation, GDM was based on the 75-g oral-glucose-tolerance test. Self-reported sleep duration was collected via the Pittsburgh Sleep Quality Index questionnaire in the second (24-28 weeks) and third (32-36 weeks) trimesters. Outcomes of neurodevelopmental delay in 6 to 36 months postpartum were evaluated using Denver Developmental Screening Test-II and Gesell Development Diagnosis Scale. Results Compared with the unexposed group, women with "GDM + SSD" have the greatest risks of child neurodevelopmental delay (hazard ratio with 95% CI: 1.58 [1.03-2.44]). "GDM + SSD" was associated with the greatest risks of maternal-fetal glucose metabolic disorder. An interquartile ratio (0.58 mmol/L) increase in cord blood C-peptide was associated with the risk of child neurodevelopmental delay (hazard ratio with 95% CI: 1.28 [1.12-1.48]). The stronger linear association of maternal glucose metabolism profiles and C-peptide in women with "GDM + SSD" was also demonstrated. The proportion of association between "GDM + SSD" and child neurodevelopmental delay mediated by C-peptide was 14.4%. Conclusion GDM complicated with SSD was associated with increased risk for child neurodevelopmental delay by enhancing the intergenerational association of maternal-fetal glucose metabolism disorder. [ABSTRACT FROM AUTHOR]