Trehalose 6-phosphate: a signal of sucrose status

2008 ◽  
Vol 412 (1) ◽  
pp. e1-e2 ◽  
Author(s):  
Matthew J. Paul
Keyword(s):  
Transgenic Plants ◽  
Plant Metabolism ◽  
Vital Function ◽  
Tissue Specific ◽  
Biochemical Journal ◽  
Specific Manner ◽  
Plant Genes ◽  
Important Regulator ◽  
Precise Role

T6P (trehalose 6-phosphate), the precursor of trehalose, has come out of obscurity over 10 years to be appreciated as an important regulator of plant metabolism and development, quite possibly linking the two. This information has been gained from analysis of mutant and transgenic plants, which show strong, diverse and strategically important phenotypes. Plant genes that encode the trehalose pathway are numerous and highly regulated transcriptionally and post-translationally, responding sensitively to the environment in a developmentally programmed and tissue-specific manner further suggestive of a vital function. Yet the precise role of T6P has not been clear. In an article published in the Biochemical Journal in 2006, John Lunn and colleagues addressed a major obstacle to understanding the function of T6P through development of a method capable of resolving femtomolar quantities of T6P from very small amounts of tissue. Using this technology, the authors showed large changes in T6P content that reflect tissue sucrose status. Overall, this elegant work makes an important contribution towards our understanding of the function of T6P in plants.

scholarly journals Tissue-Specific Differences of p53 Inhibition by Mdm2 and Mdm4

2006 ◽  
Vol 26 (1) ◽  
pp. 192-198 ◽  
Author(s):  
Jason D. Grier ◽  
Shunbin Xiong ◽  
Ana C. Elizondo-Fraire ◽  
John M. Parant ◽  
Guillermina Lozano
Keyword(s):  
Heart Failure ◽  
Heart Development ◽  
Direct Evidence ◽  
Critical Number ◽  
Tissue Specific ◽  
Embryonic Lethal ◽  
Proliferation And Apoptosis ◽  
Specific Manner ◽  
Correct Ratio

ABSTRACT The function of the p53 tumor suppressor to inhibit proliferation or initiate apoptosis is often abrogated in tumor cells. Mdm2 and its homolog, Mdm4, are critical inhibitors of p53 that are often overexpressed in human tumors. In mice, loss of Mdm2 or Mdm4 leads to embryonic lethal phenotypes that are completely rescued by concomitant loss of p53. To examine the role of Mdm2 and Mdm4 in a temporal and tissue-specific manner and to determine the relationships of these inhibitors to each other, we generated conditional alleles. We deleted Mdm2 and Mdm4 in cardiomyocytes, since proliferation and apoptosis are important processes in heart development. Mice lacking Mdm2 in the heart were embryonic lethal and showed defects at the time recombination occurred. A critical number of cardiomyocytes were lost by embryonic day 13.5, resulting in heart failure. This phenotype was completely rescued by deletion of p53. Mice lacking Mdm4 in the heart were born at the correct ratio and appeared to be normal. Our studies provide the first direct evidence that Mdm2 can function in the absence of Mdm4 to regulate p53 activity in a tissue-specific manner. Moreover, Mdm4 cannot compensate for the loss of Mdm2 in heart development.

scholarly journals Ciliary and extraciliary Gpr161 pools repress hedgehog signaling in a tissue-specific manner

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Sun-Hee Hwang ◽  
Bandarigoda N Somatilaka ◽  
Kevin White ◽  
Saikat Mukhopadhyay
Keyword(s):  
G Protein ◽  
Neural Tube ◽  
Hedgehog Signaling ◽  
Primary Cilia ◽  
Camp Signaling ◽  
Tissue Specific ◽  
Specific Manner ◽  
G Protein Coupled ◽  
Ciliary Localization

The role of compartmentalized signaling in primary cilia during tissue morphogenesis is not well understood. The cilia-localized G-protein-coupled receptor—Gpr161 represses hedgehog pathway via cAMP signaling. We engineered a knock-in at Gpr161 locus in mice to generate a variant (Gpr161mut1), which was ciliary localization defective but cAMP signaling competent. Tissue phenotypes from hedgehog signaling depend on downstream bifunctional Gli transcriptional factors functioning as activators/repressors. Compared to knockout (ko), Gpr161mut1/ko had delayed embryonic lethality, moderately increased hedgehog targets and partially down-regulated Gli3-repressor. Unlike ko, the Gpr161mut1/ko neural tube did not show Gli2-activator-dependent expansion of ventral-most progenitors. Instead, the intermediate neural tube showed progenitor expansion that depends on loss of Gli3-repressor. Increased extraciliary receptor (Gpr161mut1/mut1) prevented ventralization. Morphogenesis in limb buds and midface requires Gli-repressor; these tissues in Gpr161mut1/mut1 manifested hedgehog hyperactivation phenotypes—polydactyly and midfacial widening. Thus, ciliary and extraciliary Gpr161 pools likely establish tissue-specific Gli-repressor thresholds in determining morpho-phenotypic outcomes.

scholarly journals Regulation of BMP4/Dpp retrotranslocation and signaling by deglycosylation

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Antonio Galeone ◽  
Joshua M Adams ◽  
Shinya Matsuda ◽  
Maximiliano F Presa ◽  
Ashutosh Pandey ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Secretory Pathway ◽  
Proteasomal Degradation ◽  
Bmp Signaling ◽  
Tissue Specific ◽  
Biologically Relevant ◽  
Endoplasmic Reticulum Associated Degradation ◽  
Specific Manner

During endoplasmic reticulum-associated degradation (ERAD), the cytoplasmic enzyme N-glycanase 1 (NGLY1) is proposed to remove N-glycans from misfolded N-glycoproteins after their retrotranslocation from the ER to the cytosol. We previously reported that NGLY1 regulates Drosophila BMP signaling in a tissue-specific manner (Galeone et al., 2017). Here, we establish the Drosophila Dpp and its mouse ortholog BMP4 as biologically relevant targets of NGLY1 and find, unexpectedly, that NGLY1-mediated deglycosylation of misfolded BMP4 is required for its retrotranslocation. Accumulation of misfolded BMP4 in the ER results in ER stress and prompts the ER recruitment of NGLY1. The ER-associated NGLY1 then deglycosylates misfolded BMP4 molecules to promote their retrotranslocation and proteasomal degradation, thereby allowing properly-folded BMP4 molecules to proceed through the secretory pathway and activate signaling in other cells. Our study redefines the role of NGLY1 during ERAD and suggests that impaired BMP4 signaling might underlie some of the NGLY1 deficiency patient phenotypes.

Hypertension Increases Connexin43 in a Tissue-Specific Manner

Circulation ◽  
1997 ◽  
Vol 95 (4) ◽  
pp. 1007-1014 ◽  
Author(s):  
Jacques-Antoine Haefliger ◽  
Einar Castillo ◽  
Ge´rard Waeber ◽  
Gabriela E. Bergonzelli ◽  
Jean-Franc¸ois Aubert ◽  
...  
Keyword(s):  
Tissue Specific ◽  
Specific Manner

scholarly journals Tentacle Morphological Variation Coincides with Differential Expression of Toxins in Sea Anemones

Toxins ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 452
Author(s):  
Lauren M. Ashwood ◽  
Michela L. Mitchell ◽  
Bruno Madio ◽  
David A. Hurwood ◽  
Glenn F. King ◽  
...  
Keyword(s):  
Differential Expression ◽  
Morphological Variation ◽  
Expression Profiles ◽  
The Body ◽  
Sea Anemones ◽  
Tissue Specific ◽  
Venom Composition ◽  
Specific Manner ◽  
Branched Structures ◽  
Morphological Variants

Phylum Cnidaria is an ancient venomous group defined by the presence of cnidae, specialised organelles that serve as venom delivery systems. The distribution of cnidae across the body plan is linked to regionalisation of venom production, with tissue-specific venom composition observed in multiple actiniarian species. In this study, we assess whether morphological variants of tentacles are associated with distinct toxin expression profiles and investigate the functional significance of specialised tentacular structures. Using five sea anemone species, we analysed differential expression of toxin-like transcripts and found that expression levels differ significantly across tentacular structures when substantial morphological variation is present. Therefore, the differential expression of toxin genes is associated with morphological variation of tentacular structures in a tissue-specific manner. Furthermore, the unique toxin profile of spherical tentacular structures in families Aliciidae and Thalassianthidae indicate that vesicles and nematospheres may function to protect branched structures that host a large number of photosynthetic symbionts. Thus, hosting zooxanthellae may account for the tentacle-specific toxin expression profiles observed in the current study. Overall, specialised tentacular structures serve unique ecological roles and, in order to fulfil their functions, they possess distinct venom cocktails.

scholarly journals Cholinergic Signaling, Neural Excitability, and Epilepsy

Molecules ◽  
2021 ◽  
Vol 26 (8) ◽  
pp. 2258
Author(s):  
Yu Wang ◽  
Bei Tan ◽  
Yi Wang ◽  
Zhong Chen
Keyword(s):  
Cholinergic Neurons ◽  
Epileptic Seizures ◽  
Brain Disorder ◽  
Neural Excitability ◽  
Cholinergic Signaling ◽  
The Central Nervous System ◽  
Muscarinic And Nicotinic Receptors ◽  
Cumulative Evidence ◽  
Precise Role

Epilepsy is a common brain disorder characterized by recurrent epileptic seizures with neuronal hyperexcitability. Apart from the classical imbalance between excitatory glutamatergic transmission and inhibitory γ-aminobutyric acidergic transmission, cumulative evidence suggest that cholinergic signaling is crucially involved in the modulation of neural excitability and epilepsy. In this review, we briefly describe the distribution of cholinergic neurons, muscarinic, and nicotinic receptors in the central nervous system and their relationship with neural excitability. Then, we summarize the findings from experimental and clinical research on the role of cholinergic signaling in epilepsy. Furthermore, we provide some perspectives on future investigation to reveal the precise role of the cholinergic system in epilepsy.

scholarly journals Role of DegQ in differential stability of flagellin subunits in Vibrio vulnificus

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
You-Chul Jung ◽  
Mi-Ae Lee ◽  
Han-Shin Kim ◽  
Kyu-Ho Lee
Keyword(s):  
Life Cycle ◽  
Biofilm Formation ◽  
Vibrio Vulnificus ◽  
Differential Regulation ◽  
Specific Manner ◽  
Associated Proteins ◽  
Differential Stability ◽  
Methionine Residues

AbstractBiofilm formation of Vibrio vulnificus is initiated by adherence of flagellated cells to surfaces, and then flagellum-driven motility is not necessary during biofilm maturation. Once matured biofilms are constructed, cells become flagellated and swim to disperse from biofilms. As a consequence, timely regulations of the flagellar components’ expression are crucial to complete a biofilm life-cycle. In this study, we demonstrated that flagellins’ production is regulated in a biofilm stage-specific manner, via activities of a protease DegQ and a chaperone FlaJ. Among four flagellin subunits for V. vulnificus filament, FlaC had the highest affinities to hook-associated proteins, and is critical for maturating flagellum, showed the least susceptibility to DegQ due to the presence of methionine residues in its DegQ-sensitive domains, ND1 and CD0. Therefore, differential regulation by DegQ and FlaJ controls the cytoplasmic stability of flagellins, which further determines the motility-dependent, stage-specific development of biofilms.

scholarly journals Syntaxin 1A Gene Is Negatively Regulated in a Cell/Tissue Specific Manner by YY1 Transcription Factor, Which Binds to the −183 to −137 Promoter Region Together with Gene Silencing Factors Including Histone Deacetylase

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 146
Author(s):  
Takahiro Nakayama ◽  
Toshiyuki Fukutomi ◽  
Yasuo Terao ◽  
Kimio Akagawa
Keyword(s):  
Transcription Factor ◽  
Gene Silencing ◽  
Protein Complex ◽  
Promoter Region ◽  
Neuronal Cell ◽  
Syntaxin 1A ◽  
Tissue Specific ◽  
Cell Tissue ◽  
Specific Manner ◽  
A Cell

The HPC-1/syntaxin 1A (Stx1a) gene, which is involved in synaptic transmission and neurodevelopmental disorders, is a TATA-less gene with several transcription start sites. It is activated by the binding of Sp1 and acetylated histone H3 to the −204 to +2 core promoter region (CPR) in neuronal cell/tissue. Furthermore, it is depressed by the association of class 1 histone deacetylases (HDACs) to Stx1a–CPR in non-neuronal cell/tissue. To further clarify the factors characterizing Stx1a gene silencing in non-neuronal cell/tissue not expressing Stx1a, we attempted to identify the promoter region forming DNA–protein complex only in non-neuronal cells. Electrophoresis mobility shift assays (EMSA) demonstrated that the −183 to −137 OL2 promoter region forms DNA–protein complex only in non-neuronal fetal rat skin keratinocyte (FRSK) cells which do not express Stx1a. Furthermore, the Yin-Yang 1 (YY1) transcription factor binds to the −183 to −137 promoter region of Stx1a in FRSK cells, as shown by competitive EMSA and supershift assay. Chromatin immunoprecipitation assay revealed that YY1 in vivo associates to Stx1a–CPR in cell/tissue not expressing Stx1a and that trichostatin A treatment in FRSK cells decreases the high-level association of YY1 to Stx1a-CPR in default. Reporter assay indicated that YY1 negatively regulates Stx1a transcription. Finally, mass spectrometry analysis showed that gene silencing factors, including HDAC1, associate onto the −183 to −137 promoter region together with YY1. The current study is the first to report that Stx1a transcription is negatively regulated in a cell/tissue-specific manner by YY1 transcription factor, which binds to the −183 to −137 promoter region together with gene silencing factors, including HDAC.

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