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Light and boron play a significant role in the physiological growth and yield of crops such as groundnut. Even so, there has been little information on the application of boron in groundnut, while no information is available in Bangladesh regarding the imposition of light in groundnut. Therefore, two field experiments were conducted in order to evaluate the physiological growth and seed yield of groundnut. Treatments included two levels of light, viz ., L 0 = normal day length (≈12-h light) and L = normal day length + 6-h extended light at night (≈18-h light); three levels of boron, viz ., 0-kg B ha -1 (B 0 ), 1-kg B ha- 1 (B 1 ) and 2-kg B ha -1 (B 2 ), and two groundnut varieties, viz ., V 1 = ‘Dhaka-1’ and V 2 = ‘BARI Chinabadam-8’. The results obtained from the experiment revealed that the highest LAI, LAR, LMR and RWR were recorded in L, B 2 and V 2 variants, while NAR was the highest in L 0 and B 0 . Moreover, it was noted an inconsistent result for RGR found for boron application. Based on the results, it could be concluded that boron is one of the factors responsible for higher yield of groundnut; nevertheless, under the extended light, it is not possible to get the highest yield.

Hypoxia plays a role in the deterioration of β-cell function. Hepatocyte nuclear factor 4α (HNF4α) has an important role in pancreatic β-cells, and mutations of the human HNF4A gene cause a type of maturity-onset diabetes of the young (MODY1). However, it remains unclear whether hypoxia affects the expression of HNF4α in β-cells. Here, we report that hypoxia reduces HNF4α protein expression in β-cells. Hypoxia-inducible factor was not involved in the down-regulation of HNF4α under hypoxic conditions. The down-regulation of HNF4α was dependent on the activation of AMP-activated protein kinase (AMPK), and the reduction of HNF4α protein expression by metformin, an AMPK activator, and hypoxia was inhibited by the overexpression of a kinase-dead (KD) form of AMPKα2. In addition, hypoxia decreased the stability of the HNF4α protein, and the down-regulation of HNF4α was sensitive to proteasome inhibitors. Adenovirus-mediated overexpression of KD-AMPKα2 improved insulin secretion in metformin-treated islets, hypoxic islets, and ob/ob mouse islets. These results suggest that down-regulation of HNF4α could be of importance in β-cell dysfunction by hypoxia.

Sirtuin 7 (SIRT7) is an NAD+-dependent deacetylase/deacylase, but only a limited number of SIRT7 substrates have been identified. Recently, we found that Sirt7 knockout mice are resistant to high-fat diet-induced fatty liver, and that SIRT7 positively regulates the protein level of TR4, a nuclear receptor involved in lipid metabolism, by inhibiting the CUL4B/DDB1/DCAF1 E3 ubiquitin ligase complex. However, the mechanism by which SIRT7 inhibits the E3 ubiquitin ligase complex was not identified. Here, we demonstrate that SIRT7 binds directly to DDB1 and deacetylates DDB1 at Lys1121. K1121R-DDB1 (a deacetylation-mimicking mutant) displayed reduced binding with DCAF1. The expression of TR4 protein and TR4 target genes, including Cd36, Cidea, Cidec and Pparg1, was increased in K1121R-DDB1-overexpressing Hepa1-6 cells compared to WT-DDB1-overexpressing cells. Our results indicate that the SIRT7-mediated deacetylation of K1121 attenuates the activity of the CUL4B/DDB1/DCAF1 E3 ubiquitin ligase complex by reducing binding between DDB1 and DCAF1, leading to the increased expression of TR4.

Sirt7 localizes in the nucleus (enriched in the nucleolus) and is an NAD(+)-dependent deacetylase with high selectivity for the acetylated lysine 18 of histone H3 (H3K18Ac). It has been reported that Sirt7 is necessary for maintaining the fundamental properties of the cancer cell phenotype and stabilizing the tumorigenicity of human cancer via deacetylation of H3K18Ac. However, the regulators of Sirt7 deacetylase activity are unknown. Myb-binding protein 1a (Mybbp1a) is reported to interact with and regulate the function of a number of transcription factors. In the present study, we demonstrated that Mybbp1a binds to Sirt7 in vitro and in vivo. Serial deletion studies indicated that N- and C-terminal regions of Sirt7 and C-terminal region of Mybbp1a are important for the binding. Furthermore, transfection experiments showed that Mybbp1a is capable of inhibiting the deacetylation activity of H3K18Ac by Sirt7. Our findings demonstrate that Mybbp1a is a novel negative regulator of Sirt7.

Patchouli oil, an essential aroma oil extracted from patchouli leaf during short-term exposure with five and ten drops either inhibited (at 1 or 2 h) or stimulated (at 4 h) the platelet MAO-A activity depending on the dosages of the aroma oil mainly due to inhibition or stimulation of its K m. The long-term 15 consecutive days exposure (with two or five drops) of patchouli oil, on the other hand, maximally stimulated the platelet MAO-A activity with five drops patchouli oil for 1 h exposure, but further continuation of its exposure with same doses (two or five drops) for 30 consecutive days significantly stimulated (with two drops) and inhibited (with five drops) the platelet MAO-A activity due to stimulation and inhibition respectively of its corresponding both K m and V max. These results thus suggest that this aroma oil exposure may modulate the blood platelet serotonergic regulation depending on the dose, duration, and conditions of exposure.

Boron is an important micronutrient that enhances vegetative growth and yield of crops, like peanut. Light also plays an important role in pegging of peanut. There has been little information regarding the application of boron and light in peanut in Bangladesh. Therefore, a field experiment was conducted to study the response of boron and light on morph-physiology and pod yield of two peanut varieties. Treatments considered two peanut varieties,namely, Dhaka-1 and BARI Chinabadam-8, three levels of boron (B),namely, 0-kg B ha−1(B0), 1-kg B ha−1(B1), and 2-kg B ha−1(B2), and two levels of light,namely, normal day light (≈12 h light) and normal day light + 6 h extended red light at night (≈18 h light). Result revealed that days to first-last emergence and days to first-50% flowering took shorter times and vegetative growth, pods dry weight plant−1, pod yield, and germination were markedly increased with the application of boron. Vegetative growth and germinations were significantly increased in light, but the lowest leaf area, pods dry weight plant−1, and pod yield were found in light. Without germination, the highest vegetative growth, reproductive unit, and pod yield were observed from BARI Chinabadam-8. Days to first-last emergence, days to first-50% flowering, and number of branches plant−1were found linearly related to pod yield.

High‐sensitivity C‐reactive protein (hs‐CRP) levels in European populations are lower in patients with maturity‐onset diabetes of the young type 3 (MODY3) than in those with type 2 diabetes. hs‐CRP levels have been suggested to be useful for discriminating MODY3 from type 2 diabetes. As hs‐CRP levels are influenced by various factors including race and body mass index, it is worthwhile to examine whether hs‐CRP can serve as a biomarker for MODY3 in Japanese. Here we describe the case of a Japanese MODY3 patient with a nonsense mutation in the HNF1A gene. Two measurements showed consistently lower hs‐CRP levels (

SummarySirtuins (SIRT1-7) have attracted considerable attention as regulators of metabolism over the past decade. However, the physiological functions and molecular mechanisms of SIRT7 are poorly understood. Here we demonstrate that Sirt7 knockout mice were resistant to high-fat diet-induced fatty liver, obesity, and glucose intolerance, and that hepatic triglyceride accumulation was also attenuated in liver-specific Sirt7 knockout mice. Hepatic SIRT7 positively regulated the protein level of TR4/TAK1, a nuclear receptor involved in lipid metabolism, and as a consequence activated TR4 target genes to increase fatty acid uptake and triglyceride synthesis/storage. Biochemical studies revealed that the DDB1-CUL4-associated factor 1 (DCAF1)/damage-specific DNA binding protein 1 (DDB1)/cullin 4B (CUL4B) E3 ubiquitin ligase complex interacted with TR4, leading to its degradation, while binding of SIRT7 to the DCAF1/DDB1/CUL4B complex inhibited the degradation of TR4. In conclusion, we propose that hepatic SIRT7 controls lipid metabolism in liver by regulating the ubiquitin-proteasome pathway.

Mutations of the HNF4A gene cause a form of maturity-onset diabetes of the young (MODY1) that is characterized by impairment of pancreatic β-cell function. HNF4α is a transcription factor belonging to the nuclear receptor superfamily (NR2A1), but its target genes in pancreatic β-cells are largely unknown. Here, we report that ankyrin repeat and sterile α motif domain containing 4b (Anks4b) is a target of HNF4α in pancreatic β-cells. Expression of Anks4b was decreased in both βHNF4α KO islets and HNF4α knockdown MIN6 β-cells, and HNF4α activated Anks4b promoter activity. Anks4b bound to glucose-regulated protein 78 (GRP78), a major endoplasmic reticulum (ER) chaperone protein, and overexpression of Anks4b enhanced the ER stress response and ER stress-associated apoptosis of MIN6 cells. Conversely, suppression of Anks4b reduced β-cell susceptibility to ER stress-induced apoptosis. These results indicate that Anks4b is a HNF4α target gene that regulates ER stress in β-cells by interacting with GRP78, thus suggesting that HNF4α is involved in maintenance of the ER.