Leaf angle (LA) is a critical agronomic trait in maize, with more upright leaves allowing higher planting density, leading to more efficient light capture and higher yields. A few genes responsible for variation in LA have been identified by map-based cloning. In this study, we cloned maize ZmIBH1-1, which encodes a bHLH transcription factor with both a basic binding region and a helix-loop-helix domain, and the results of qRT-PCR showed that it is a negative regulator of LA. Histological analysis indicated that changes in LA were mainly caused by differential cell wall lignification and cell elongation in the ligular region. To determine the regulatory framework of ZmIBH1-1, we conducted RNA-seq and DNA affinity purification (DAP)-seq analyses. The combined results revealed 59 ZmIBH1-1-modulated target genes with annotations, and they were mainly related to the cell wall, cell development, and hormones. Based on the data, we propose a regulatory model for the control of plant architecture by ZmIBH1-1 in maize.

No abstract

Flowering time is an important agronomic trait that determines the distribution and adaptation of plants. The accurate prediction of flowering time in elite germplasm is very critical for maize breeding. However, the molecular mechanisms underlying photoperiod response remain elusive in maize. Here we cloned the flowering time controlling gene, ZmNF-YC2, by map-based cloning and confirmed that ZmNF-YC2 is the protein of nuclear transcription factor Y subunit C-2 and a positive regulator of flowering time in maize under long-day conditions. Our results show that ZmNF-YC2 promotes the expression of ZmNF-YA3. ZmNF-YA3 negatively regulates the transcription of ZmAP2. ZmAP2 suppresses the expression of ZMM4 to delay flowering time. Then we developed a gene regulatory model of flowering time in maize using ZmNF-YC2, ZmNF-YA3, ZmAP2, ZMM4 and other key genes. The cascading regulation of ZmNF-YC2 on maize flowering time has not been reported in other species.

Rationale:Cataracts can occur in children and adolescents with Type 1 Diabetes Mellitus who have poorly controlled glycemia. Here, we report a case of a 16-year-old female, who was diagnosed with bilateral cataracts, and genetic screening identified a mutation in the PRRC2A gene which is rarely reported. After surgery, retinopathy was found in this patient, combined with the published literature, we encourage that postoperative monitoring for retinal lesions during the follow-up visits should be conducted.Patient concerns:In this article, we present an adolescent diagnosed with bilateral cataracts, and developed retinopathy during the follow-up visits. Genetic screening identified a mutation in the PRRC2A gene.Diagnoses:The diagnoses of Diabetic cataracts, Type 1 diabetes and Diabetic retinopathy was made.Interventions:The patient underwent surgery in both eyes, and hypoglycemic treatment was provided.Outcomes:The surgery achieved satisfactory results, during the follow-up visits, her visual acuity was reported as 0.8 in the right eye and 1.0 in the left eye. Besides, her blood glucose was well controlled, and her glycated hemoglobin was reduced to 6.9% after three months of continuous treatment.Lessons:This case highlights the importance of genetic screening for detecting mutations in diabetes-related genes, and postoperative monitoring for retinal lesions during the follow-up visits.

Iridium/Brønsted acid cooperative catalyzed asymmetric allylic substitution reactions at the C5 position of indolines have been reported for the first time. The highly efficient protocol allows rapid access to various C5-allylated products in good to high yields (48−97%) and enantioselectivities (82% to >99% ee) with wide functional group tolerance. The transformations allow not only the formation of C5-allylindoline derivatives but also the synthesis of C5-allylindole analogues in good yields and excellent stereoselectivities via an allylation/oxidation reaction sequence.

No abstract

Leaf angle is an important agronomic trait in cereals and shares a close relationship with crop architecture and grain yield. Although it has been previously reported that ZmCLA4 can influence leaf angle, the underlying mechanism remains unclear. In this study, we used the Gal4-LexA/UAS system and transactivation analysis to demonstrate in maize (Zea mays) that ZmCLA4 is a transcriptional repressor that regulates leaf angle. DNA affinity purification sequencing (DAP-Seq) analysis revealed that ZmCLA4 mainly binds to promoters containing the EAR motif (CACCGGAC) as well as to two other motifs (CCGARGS and CDTCNTC) to inhibit the expression of its target genes. Further analysis of ZmCLA4 target genes indicated that ZmCLA4 functions as a hub of multiple plant hormone signaling pathways: ZmCLA4 was found to directly bind to the promoters of multiple genes including ZmARF22 and ZmIAA26 in the auxin transport pathway, ZmBZR3 in the brassinosteroid signaling pathway, two ZmWRKY genes involved in abscisic acid metabolism, ZmCYP genes (ZmCYP75B1, ZmCYP93D1) related to jasmonic acid metabolism, and ZmABI3 involved in the ethylene response pathway. Overall, our work provides deep insights into the ZmCLA4 regulatory network in controlling leaf angle in maize.

Several studies have shown that active smoking is a risk factor for type 2 diabetes mellitus (T2DM). However, the effects of passive smoking on T2DM remains unknown. In this study, we investigated the effects of passive smoking and its duration on the prevalence of prediabetes and T2DM. According to passive smoking status, participants were divided into Group A (passive smokers) and Group B (controls). Furthermore, Group A was divided into three subgroups according to the duration of passive smoking: Group A1 (≤10 years), Group A2 (10-20 years), and Group A3 (>20 years). We found that the prevalence of impaired glucose tolerance (IGT) in Group A (26.6%), Group A2 (28%), and Group A3 (37.8%) was significantly higher than that in Group B (19.6%), and the prevalence gradually increased with an increase in the duration of passive smoking. Multiple logistic regression analysis showed that passive smoking for >10 years was a risk factor for impaired fasting glucose (IFG), IGT, and T2DM. Therefore, passive smoking not only increases the prevalence of IGT in a time-dependent manner, but also a risk factor for IFG, IGT, and T2DM when its duration is over 10 years.