scholarly journals The Thiol Reductase Activity of YUCCA6 Mediates Delayed Leaf Senescence by Regulating Genes Involved in Auxin Redistribution

2016 ◽  
Vol 7 ◽  
Author(s):  
Joon-Yung Cha ◽  
Mi R. Kim ◽  
In J. Jung ◽  
Sun B. Kang ◽  
Hee J. Park ◽  
...  
2009 ◽  
Vol 20 (16) ◽  
pp. 3628-3637 ◽  
Author(s):  
Philippe J. Nadeau ◽  
Steve J. Charette ◽  
Jacques Landry

ASK1 cysteine oxidation allows JNK activation upon oxidative stress. Trx1 negatively regulates this pathway by reducing the oxidized cysteines of ASK1. However, precisely how oxidized ASK1 is involved in JNK activation and how Trx1 regulates ASK1 oxidoreduction remains elusive. Here, we describe two different thiol reductase activities of Trx1 on ASK1. First, in H2O2-treated cells, Trx1 reduces the various disulfide bonds generated between cysteines of ASK1 by a rapid and transient action. Second, in untreated cells, Trx1 shows a more stable thiol reductase activity on cysteine 250 (Cys250) of ASK1. After H2O2 treatment, Trx1 dissociates from Cys250, which is not sufficient to activate the ASK1-JNK pathway. Indeed, in untreated cells, a Cys250 to alanine mutant of ASK1 (C250A), which cannot bind Trx1, does not constitutively activate JNK. On the other hand, in H2O2-treated cells, this mutant (C250A) fails to activate JNK and does not induce apoptosis, although it remains fully phosphorylated on Threonine 838 (Thr838) in its activation loop. Overall, our data show that Cys250 is essential for H2O2-dependent signaling downstream from ASK1 but at a step subsequent to the phosphorylation of ASK1 Thr838. They also clarify the thiol reductase function of Trx1 on ASK1 activity.


2009 ◽  
Vol 109 (10) ◽  
pp. 2297-2307 ◽  
Author(s):  
Yukiko Sakimoto ◽  
Kimihiko Hirao ◽  
Djamaladdin G. Musaev

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Joon-Yung Cha ◽  
Woe-Yeon Kim ◽  
Sun Bin Kang ◽  
Jeong Im Kim ◽  
Dongwon Baek ◽  
...  

2010 ◽  
Vol 135 (2) ◽  
pp. 108-115 ◽  
Author(s):  
Yan Zhang ◽  
Cuiyue Liang ◽  
Yan Xu ◽  
Thomas Gianfagna ◽  
Bingru Huang

The objective of the study was to determine whether the expression of a cytokinin (CK) biosynthesis gene encoding adenine isopentenyl transferase (ipt) would delay or suppress leaf senescence induced by nitrogen (N) or phosphorus (P) deficiency in a C3 grass species, creeping bentgrass (Agrostis stolonifera). The ipt gene was ligated to a senescence-associated promoter, SAG12, and was transferred into creeping bentgrass using an agrobacterium (Agrobacterium tumefaciens)-mediated transformation technique. Plants from an SAG12-ipt transgenic line (S41) and a null transformant (NT) control line were grown in nutrient solutions with all essential elements or without N (−N) or P (−P) for 21 days. Significant declines in leaf photochemical efficiency (Fv/Fm) and chlorophyll content of mature leaves were detected in NT and SAG12-ipt plants exposed to N or P deficiency. Compared to the NT control line, SAG12-ipt plants had higher levels of Fv/Fm, chlorophyll, and CK contents in leaves, and these differences between the NT control and SAG12-ipt line became more pronounced with treatment duration. The ipt expression was detected in the −P-treated and the −N-treated plants after 21 days, although the level of expression decreased under N or P deficiency. Under −P treatment, root acid phosphatase activity was greater in SAG12-ipt line than in the NT control line. No significant differences in nitrate reductase activity were detected in leaves or roots between the SAG12-ipt and the NT control lines. Our results demonstrated that SAG12-ipt expression suppressed leaf senescence induced by N or P deficiency in a perennial grass species. The suppressing effects on leaf senescence under P deficiency may be related to CK regulation of more efficient use of P in roots of the SAG12-ipt plants.


2021 ◽  
Vol 15 (11) ◽  
pp. e0009958
Author(s):  
Hong Fei ◽  
Muhammad Ali-ul-Husnain Naqvi ◽  
Sana Zahra Naqvi ◽  
Lixin Xu ◽  
Xiaokai Song ◽  
...  

Trichinella spiralis is mammalian skeletal muscles parasite which may cause trichinellosis in animals and humans. Gamma interferon inducible lysosomal thiol reductase (GILT) is a widespread superfamily which plays key role in processing and presentation of MHC class II restricted antigen by catalyzing disulfide bond reduction. There are no reports about GILT in T. spiralis. In present study, GILT from T. spiralis (Tsp-GILT) was cloned, analyzed by multiple-sequence alignment, and predicted by 3D structure model. Recombinant Tsp-GILT (about 46 kDa) was efficiently expressed in Escherichia coli and thiol reductase activity suggested that in acidic environment the addition of a reducing agent is needed. Soaking method was used to knockdown expression of Tsp-GILT using small interference RNA (siRNA). Immunofluorescence assay confirmed the transformation of siRNA into muscle larva (ML) and new born larva (NBL). Quantitative real time-PCR (QRT-PCR) analysis revealed that transcription level of Tsp-GILT mRNA can be up-regulated by stimulation of mouse IFN-γ and down-regulated by siRNA2 in vitro. NBLs soaked with siRNA2 showed 32.3% reduction in the generation of MLs. MLs soaked with siRNA2 showed 26.2% reduction in the next generation of MLs, but no significant effect was observed on adult worms or NBLs. These findings concluded that GILT may play important roles in the development of T. spiralis parasite.


2020 ◽  
Vol 477 (14) ◽  
pp. 2715-2720
Author(s):  
Susana Castro-Obregón

The nuclear envelope is composed by an outer nuclear membrane and an inner nuclear membrane, which is underlain by the nuclear lamina that provides the nucleus with mechanical strength for maintaining structure and regulates chromatin organization for modulating gene expression and silencing. A layer of heterochromatin is beneath the nuclear lamina, attached by inner nuclear membrane integral proteins such as Lamin B receptor (LBR). LBR is a chimeric protein, having also a sterol reductase activity with which it contributes to cholesterol synthesis. Lukasova et al. showed that when DNA is damaged by ɣ-radiation in cancer cells, LBR is lost causing chromatin structure changes and promoting cellular senescence. Cellular senescence is characterized by terminal cell cycle arrest and the expression and secretion of various growth factors, cytokines, metalloproteinases, etc., collectively known as senescence-associated secretory phenotype (SASP) that cause chronic inflammation and tumor progression when they persist in the tissue. Therefore, it is fundamental to understand the molecular basis for senescence establishment, maintenance and the regulation of SASP. The work of Lukasova et al. contributed to our understanding of cellular senescence establishment and provided the basis that lead to the further discovery that chromatin changes caused by LBR reduction induce an up-regulated expression of SASP factors. LBR dysfunction has relevance in several diseases and possibly in physiological aging. The potential bifunctional role of LBR on cellular senescence establishment, namely its role in chromatin structure together with its enzymatic activity contributing to cholesterol synthesis, provide a new target to develop potential anti-aging therapies.


Sign in / Sign up

Export Citation Format

Share Document