SummaryKernel size‐related traits are the most direct traits correlating with grain yield. The genetic basis of three kernel traits of maize, kernel length (KL), kernel width (KW) and kernel thickness (KT), was investigated in an association panel and a biparental population. A total of 21 single nucleotide polymorphisms (SNPs) were detected to be most significantly (P < 2.25 × 10−6) associated with these three traits in the association panel under four environments. Furthermore, 50 quantitative trait loci (QTL) controlling these traits were detected in seven environments in the intermated B73 × Mo17 (IBM) Syn10 doubled haploid (DH) population, of which eight were repetitively identified in at least three environments. Combining the two mapping populations revealed that 56 SNPs (P < 1 × 10−3) fell within 18 of the QTL confidence intervals. According to the top significant SNPs, stable‐effect SNPs and the co‐localized SNPs by association analysis and linkage mapping, a total of 73 candidate genes were identified, regulating seed development. Additionally, seven miRNAs were found to situate within the linkage disequilibrium (LD) regions of the co‐localized SNPs, of which zma‐miR164e was demonstrated to cleave the mRNAs of Arabidopsis CUC1,CUC2 and NAC6 in vitro. Overexpression of zma‐miR164e resulted in the down‐regulation of these genes above and the failure of seed formation in Arabidopsis pods, with the increased branch number. These findings provide insights into the mechanism of seed development and the improvement of molecular marker‐assisted selection (MAS) for high‐yield breeding in maize.
Stem cell senescence increases alongside the progressive functional declines that characterize aging. The effects of extracellular vesicles (EVs) are now attracting intense interest in the context of aging and age-related diseases. Here, we demonstrate that neonatal umbilical cord (UC) is a source of EVs derived from mesenchymal stem cells (MSC-EVs). These UC-produced MSC-EVs (UC-EVs) contain abundant anti-aging signals and rejuvenate senescing adult bone marrow–derived MSCs (AB-MSCs). UC-EV–rejuvenated AB-MSCs exhibited alleviated aging phenotypes and increased self-renewal capacity and telomere length. Mechanistically, UC-EVs rejuvenate AB-MSCs at least partially by transferring proliferating cell nuclear antigen (PCNA) into recipient AB-MSCs. When tested in therapeutic context, UC-EV–triggered rejuvenation enhanced the regenerative capacities of AB-MSCs in bone formation, wound healing, and angiogenesis. Intravenously injected UC-EVs conferred anti-aging phenotypes including decreased bone and kidney degeneration in aged mice. Our findings reveal that UC-EVs are of high translational value in anti-aging intervention.
Insulin and (-)-epigallocatechin gallate (EGCG) have been reported to regulate fat cell mitogenesis and adipogenesis, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated mitogenesis in 3T3-L1 preadipocytes. EGCG inhibited insulin stimulation of preadipocyte proliferation in a dose- and time-dependent manner. EGCG also suppressed insulin-stimulated phosphorylation of the insulin receptor-beta, insulin receptor (IR) substrates 1 and 2 (IRS1 and IRS2), and mitogen-activated protein kinase pathway proteins, RAF1, MEK1/2, and ERK1/2, but not JNK. Furthermore, EGCG inhibited the association of IR with the IRS1 and IRS2 proteins, but not with the IRS4 protein. These data suggest that EGCG selectively affects particular types of IRS and MAPK family members. Generally, EGCG was more effective than epicatechin, epicatechin gallate, and epigallocatechin in modulating insulin-stimulated mitogenic signaling. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and found that its expression was sensitive to growth phase, tissue type, and differentiation state. Pretreatment of preadipocytes with 67LR antiserum prevented the effects of EGCG on insulin-stimulated phosphorylation of IRS2, RAF1, and ERK1/2 and insulin-stimulated preadipocyte proliferation (cell number and bromodeoxyuridine incorporation). Moreover, EGCG tended to increase insulin-stimulated associations between the 67LR and IR, IRS1, IRS2, and IRS4 proteins. These data suggest that EGCG mediates anti-insulin signaling in preadipocyte mitogenesis via the 67LR pathway.
Green tea (-)-epigallocatechin-3-gallate (EGCG) is known as to regulate obesity and fat cell activity. However, little information is known about the effects of EGCG on oxidative reactive oxygen species (ROS) of fat cells. Using 3T3-L1 preadipocytes and adipocytes, we found that EGCG increased ROS production in dose- and time-dependent manners. The concentration of EGCG that increased ROS levels by 180-500% was approximately 50 muM for a range of 8-16 h of treatment. In contrast, EGCG dose- and time-dependently decreased the amount of intracellular glutathione (GSH) levels. EGCG was more effective than (-)-epicatechin, (-)-epicatechin-3-gallate, and (-)-epigallocatechin in changing ROS and GSH levels. This suggests a catechin-specific effect. To further examine the relation of GSH to ROS as altered by EGCG, we observed that exposure of preadipocytes and adipocytes to N-acetyl-L-cysteine (a GSH precursor) blocked the EGCG-induced increases in ROS levels and decreases in GSH levels. These observations suggest a GSH-dependent effect of EGCG on ROS production. While EGCG was demonstrated to alter levels of ROS and GSH, its signaling was altered by an EGCG receptor (the so-called 67 kDa laminin receptor(67LR)) antiserum, but not by normal rabbit serum. These data suggest that EGCG mediates GSH and ROS levels via the 67LR pathway.
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