Jun‐Ho Lee

SOC1, encoding a MADS box transcription factor, integrates multiple flowering signals derived from photoperiod, temperature, hormone, and age-related signals. SOC1 is regulated by two antagonistic flowering regulators, CONSTANS (CO) and FLOWERING LOCUS C (FLC), which act as floral activator and repressor, respectively. CO activates SOC1 mainly through FT but FLC represses SOC1 by direct binding to the promoter. SOC1 is also activated by an age-dependent mechanism in which SPL9 and microRNA156 are involved. When SOC1 is induced at the shoot apex, SOC1 together with AGL24 directly activates LEAFY (LFY), a floral meristem identity gene. APETALA1 (AP1), activated mainly by FT, is also necessary to establish and maintain flower meristem identity. When LFY and AP1 are established, flower development occurs at the anlagen of shoot apical meristem according to the ABC model. During early flower development, AP1 activates the A function and represses three redundantly functioning flowering time genes, SOC1, AGL24, and SVP to prevent floral reversion. During late flower development, such repression is also necessary to activate SEPALATA3 (SEP3) which is a coactivator of B and C function genes with LFY, otherwise SEP3 is suppressed by SOC1, AGL24, and SVP. Therefore, SOC1 is necessary to prevent premature differentiation of the floral meristem.

The minimal adipose phenotype of hormone-sensitive lipase (HSL)-null mice suggested that other hormonally responsive lipase(s) were present in adipocytes. Recent studies have characterized a new adipose tissue triglyceride lipase, ATGL/PNPLA2/destnutrin/iPLA2zeta/TTS2.2 (ATGL). We had previously cloned a novel adipose-enriched transcript by differential screening and recently determined its identity with murine ATGL. We report here on the regulation of ATGL by TNF-alpha and insulin in 3T3-L1 adipocytes and identify ATGL as a target for transcriptional activation by the key adipogenic transcription factor PPARgamma. Insulin at 100 nM resulted in a marked decrease in ATGL transcript that was effectively blocked by inhibitors for PI 3-kinase and p70 ribosomal protein S6 kinase. TNF-alpha treatment decreased ATGL transcript in a time-dependent manner that paralleled TNF-alpha downregulation of PPARgamma with a maximal decrease noted by 6 h. TNF-alpha effects on ATGL were attenuated by pretreatment with PD-98059, LY-294002, or rapamycin, suggesting involvement of the p44/42 MAP kinase, PI 3-kinase, and p70 ribosomal protein S6 kinase signals. To study transcriptional regulation of ATGL, we cloned 2,979 bp of the murine ATGL 5'-flanking region. Compared with promoterless pGL2-Basic, the -2979/+21 ATGL luciferase construct demonstrated 120- and 40-fold increases in activity in white and brown adipocytes, respectively. Luciferase reporter activities for a series of eight ATGL promoter deletions revealed that the -928/+21, -1738/+21, -1979/+21, and -2979/+21 constructs were transactivated by PPARgamma. Our findings identify the novel lipase ATGL to be a target gene for TNF-alpha and insulin action in adipocytes and reveal that it is subject to transcriptional control by PPARgamma-mediated signals.

Guard cell protoplasts of Vicia faba treated with 10 [mu]M (+)abscisic acid (ABA) in the light exhibited a 20% decrease in diameter within 1.5 h, from 24.1 to 19.6 [mu]m. Within 10 s of administration of ABA, a 90% increase in levels of inositol 1,4,5-trisphosphate was observed, provided that cells were treated with Li+, an inhibitor of inositol phosphatase activity, prior to incubation. Concomitantly, levels of 32P-labeled phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-phosphate decreased 20% compared to levels in control cells; levels of label in the membrane lipids phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol did not change significantly in response to ABA treatment. These results show that phosphoinositide turnover is activated in response to ABA in guard cells. We conclude that phosphoinositide signaling is likely to be a step in the biochemical cascade that couples ABA to guard cell shrinking and stomatal closure.

// Hyunjung Baek 1 , Minsook Ye 1 , Geun-Hyung Kang 1 , Chanju Lee 1 , Gihyun Lee 1 , Da Bin Choi 1 , Jaehoon Jung 1 , Hyunseong Kim 2 , Seonhwa Lee 3 , Jin Su Kim 3 , Hyun-ju Lee 4 , Insop Shim 4 , Jun-Ho Lee 5 and Hyunsu Bae 1 1 Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea 2 K-herb Research Center, Korea Institute of Oriental Medicine, Yuseongdae-ro, Yuseong-gu, Daejeon, Republic of Korea 3 Division of RI Research, Korea Institute of Radiological & Medical Sciences University of Science & Technology, Gongneug-dong, Nowon-ku, Seoul, Republic of Korea 4 Acupuncture and Meridian Science Research Center, College of Korean Medical Science Graduate School, Kyung Hee University, Seoul, Republic of Korea 5 Department of Biotechnology, Chonnam National University, Gwangju, Republic of Korea Correspondence to: Hyunsu Bae, email: // Keywords : Alzheimer’s disease, regulatory T cells (Treg), amyloid-beta (Aβ) pathology, Immunology and Microbiology Section, Immune response, Immunity Received : July 23, 2016 Accepted : September 29, 2016 Published : October 04, 2016 Abstract Alzheimer’s disease patients display neuropathological lesions, including the accumulation of amyloid-beta (Aβ) peptide and neurofibrillary tangles. Although the mechanisms causing the neurodegenerative process are largely unknown, increasing evidence highlights a critical role of immunity in the pathogenesis of Alzheimer’s disease. In the present study, we investigated the role of regulatory T cells (Tregs) on Alzheimer’s disease progression. First, we explored the effect of Tregs (CD4 + CD25 + T cells) and Teffs (CD4 + CD25 - T cells) in an adoptive transfer model. Systemic transplantation of purified Tregs into 3xTg-AD mice improved cognitive function and reduced deposition of Aβ plaques. In contrast, adoptive transfer of Teffs diminished behavioral function and cytokine production. Next, we transiently depleted Treg population using an anti-CD25 antibody (PC61). Depletion of Tregs for four months resulted in a marked aggravation of the spatial learning deficits of six-month-old 3xTg-AD mice. Additionally, it resulted in decreasing glucose metabolism, as assessed by positron emission tomography (PET) with 18 F-2 fluoro-2-deoxy-D-glucose ([F- 18 ] FDG) neuroimaging. Importantly, the deposition of Aβ plaques and microglia/macrophage was increased in the hippocampal CA1 and CA3 regions of the Treg depleted 3xTg-AD compared to the vehicle-treated 3xTg-AD group. Our finding suggested that systemic Treg administration ameliorates disease progression and could be an effective Alzheimer’s disease treatment.