Search tips
Search criteria

Results 1-25 (57)

Clipboard (0)
Year of Publication
Document Types
1.  Protein phosphorylation-acetylation cascade connects growth factor deprivation to autophagy 
Autophagy  2012;8(9):1385-1386.
Different from unicellular organisms, metazoan cells require the presence of extracellular growth factors to utilize environmental nutrients. However, the underlying mechanism was unclear. We have delineated a pathway, in which glycogen synthase kinase 3 (GSK3) in cells deprived of growth factors phosphorylates and activates the acetyltransferase KAT5/TIP60, which in turn stimulates the protein kinase ULK1 to elicit autophagy. Cells with the Kat5/Tip60 gene replaced with Kat5S86A that cannot be phosphorylated by GSK3 are resistant to serum starvation-induced autophagy. Acetylation sites on ULK1 were mapped to K162 and K606, and the acetylation-defective mutant ULK1K162,606R displays reduced kinase activity and fails to rescue autophagy in Ulk1−/− mouse embryonic fibroblasts, indicating that acetylation is vital to the activation of ULK1. The GSK3-KAT5-ULK1 cascade seems to be specific for cells to sense growth factors, as KAT5 phosphorylation is not enhanced under glucose deprivation. Distinct from the glucose starvation-autophagy pathway that is conserved in all eukaryotic organisms, the growth factor deprivation response pathway is perhaps unique to metazoan organisms.
PMCID: PMC3442885  PMID: 22717509
GSK3; Tip60; Ulk1; acetylation; autophagy; growth factor; phosphorylation
2.  The fibroblast growth factor signaling axis controls cardiac stem cell differentiation through regulating autophagy 
Autophagy  2012;8(4):690-691.
The fibroblast growth factor (FGF) signaling axis plays important roles in heart development. Yet, the molecular mechanism by which the FGF regulates cardiogenesis is not fully understood. Using genetically engineered mouse and in vitro cultured embryoid body (EB) models, we demonstrate that FGF signaling suppresses premature differentiation of heart progenitor cells, as well as autophagy in outflow tract (OFT) myocardiac cells. The FGF also promotes mesoderm differentiation in embryonic stem cells (ESCs) but inhibits cardiomyocyte differentiation of the mesoderm cells at later stages. Furthermore, inhibition of FGF signaling increases myocardial differentiation and autophagy in both ex vivo cultured embryos and EBs, whereas activation of autophagy promotes myocardial differentiation. Thus, a link between FGF signals preventing premature differentiation of heart progenitor cells and suppression of autophagy has been established. These findings provide the first evidence that autophagy plays a role in heart progenitor differentiation, and suggest a new venue to regulate stem/progenitor cell differentiation.
PMCID: PMC3405844  PMID: 22302007
FGF; autophagy; heart defect; heart development; premature differentiation; second heart field
3.  ATM Signals miRNA Biogenesis Through KSRP 
Molecular cell  2011;41(4):367-368.
In this issue of Molecular Cell, Zhang and colleagues describe a critical link between the DNA damage response and the miRNA pathway, in which DNA double strand breaks (DSBs) induce ATM-dependent KSRP phosphorylation to facilitate pri-miRNA processing.
PMCID: PMC3075113  PMID: 21329874
4.  Degradation of the endoplasmic reticulum by autophagy in plants 
Autophagy  2013;9(4):622-623.
Eukaryotic cells have developed sophisticated strategies to contend with environmental stresses faced in their lifetime. Endoplasmic reticulum (ER) stress occurs when the accumulation of unfolded proteins within the ER exceeds the folding capacity of ER chaperones. ER stress responses have been well characterized in animals and yeast, and autophagy has been suggested to play an important role in recovery from ER stress. In plants, the unfolded protein response signaling pathways have been studied, but changes in ER morphology and ER homeostasis during ER stress have not been analyzed previously. Autophagy has been reported to function in tolerance of several stress conditions in plants, including nutrient deprivation, salt and drought stresses, oxidative stress, and pathogen infection. However, whether autophagy also functions during ER stress has not been investigated. The goal of our study was to elucidate the role and regulation of autophagy during ER stress in Arabidopsis thaliana.
PMCID: PMC3627681  PMID: 23360963
endoplasmic reticulum; autophagy; Arabidopsis; IRE1; ER stress
5.  Lipoxin A4 regulates natural killer cell and type 2 innate lymphoid cell activation in asthma 
Science translational medicine  2013;5(174):10.1126/scitranslmed.3004812.
Asthma is a prevalent disease of chronic inflammation in which endogenous counter-regulatory signaling pathways are dysregulated. Recent evidence suggests that innate lymphoid cells (ILCs), including natural killer (NK) cells and type 2 innate lymphoid cells (ILC2), can participate in the regulation of allergic airways responses, in particular airway mucosal inflammation. Here, we have identified both NK cells and ILC2 in human lung and peripheral blood in healthy and asthmatic subjects. NK cells were highly activated in severe asthma, linked to eosinophilia and interacted with autologous eosinophils to promote their apoptosis. ILC2 generated antigen-independent IL-13 in response to the mast cell product prostaglandin D2 (PGD2) alone and in a synergistic manner with the airway epithelial cytokines IL-25 and IL-33. Both NK cells and ILC2 expressed the pro-resolving ALX/FPR2 receptors. Lipoxin A4, a natural pro-resolving ligand for ALX/FPR2 receptors, significantly increased NK cell mediated eosinophil apoptosis and decreased IL-13 release by ILC2. Together, these findings indicate that ILCs are targets for lipoxin A4 to decrease airway inflammation and mediate the catabasis of eosinophilic inflammation. Because lipoxin A4 generation is decreased in severe asthma, these findings also implicate unrestrained ILC activation in asthma pathobiology.
PMCID: PMC3823369  PMID: 23447017
6.  Protective autophagy induced by RBX1/ROC1 knockdown or CRL inactivation via modulating the DEPTOR-MTOR axis 
Autophagy  2012;8(12):1856-1858.
RBX1/ROC1 is an essential subunit of the largest multiunit Cullin-RING E3 ligase (CRL), which controls the degradation of diverse substrates, thereby regulating numerous cellular processes. Recently, we reported that RBX1 is overexpressed in hepatocellular carcinomas (HCC) and its expression is negatively correlated with patient survival. Moreover, siRNA silencing of RBX1 inhibits the proliferation of liver cancer cells both in vitro and in vivo by inducing CDKN1A/p21-dependent cell senescence. Interestingly, independent of senescence, RBX1 knockdown also triggers an autophagy response, due, at least in part, to the accumulation of the MTOR-inhibitory protein DEPTOR, a recently identified CRL substrate. Biologically, blockage of autophagy significantly enhances the growth-suppressive effect of RBX1 knockdown by triggering massive apoptosis, indicating that the autophagy response upon RBX1 knockdown serves as a survival signal in liver cells. Similar observations were also made in many types of human cancer cells upon inhibition of CRL by MLN4924. These findings suggest that RBX1-CRL is a promising anti-cancer drug target and provide proof-of-concept evidence for a novel drug combination of RBX1-CRL inhibitor and autophagy inhibitor for effective treatment of human cancer.
PMCID: PMC3541304  PMID: 22965024
ROC1; RBX1; Cullin-RING E3 ligase; autophagy; senescence; DEPTOR; MTOR; neddylation; MLN4924
7.  Inactivation of the Cullin (CUL)-RING E3 ligase by the NEDD8-activating enzyme inhibitor MLN4924 triggers protective autophagy in cancer cells 
Autophagy  2012;8(11):1677-1679.
The multiunit Cullin (CUL)-RING E3 ligase (CRL) controls diverse biological processes by targeting a mass of substrates for ubiquitination and degradation, whereas its dysfunction causes carcinogenesis. Post-translational neddylation of CUL, a process triggered by the NEDD8-activating enzyme E1 subunit 1 (NAE1), is required for CRL activation. Recently, MLN4924 was discovered via a high-throughput screen as a specific NAE1 inhibitor and first-in-class anticancer drug. By blocking CUL neddylation, MLN4924 inactivates CRL and causes the accumulation of CRL substrates that trigger cell cycle arrest, senescence and/or apoptosis to suppress the growth of cancer cells in vitro and in vivo. Recently, we found that MLN4924 also triggers protective autophagy in response to CRL inactivation. MLN4924-induced autophagy is attributed partially to the inhibition of mechanistic target of rapamycin (also known as mammalian target of rapamycin, MTOR) activity by the accumulation of the MTOR inhibitory protein DEPTOR, as well as reactive oxygen species (ROS)-induced stress. Moreover, the blockage of autophagy response enhances apoptosis in MLN4924-treated cells. Together, our findings not only reveal autophagy as a novel cellular response to CRL inactivation by MLN4924, but also provide a piece of proof-of-concept evidence for the combination of MLN4924 with autophagy inhibitors to enhance therapeutic efficacy.
PMCID: PMC3494597  PMID: 22874562
Cullin-RING E3 ligase; SKP1-Cullin-F-box (SCF) E3 ligase; neddylation; NEDD8-activating enzyme; MLN4924; autophagy; DEPTOR; MTOR
8.  Does the Goldilocks Principle apply to calcium release restitution in heart cells? 
Journal of molecular and cellular cardiology  2011;52(1):10.1016/j.yjmcc.2011.10.014.
PMCID: PMC3814211  PMID: 22056316
9.  The bipolar–depressive continuum in the National Epidemiologic Survey on Alcohol and Related Conditions 
Bipolar disorders  2012;15(1):10.1111/bdi.12030.
PMCID: PMC3811045  PMID: 23231326
bipolar disorder; classification; depression
10.  When push comes to shove: SWI/SNF uses a nucleosome to get rid of a nucleosome 
Molecular cell  2010;38(4):484-486.
A report in this issue of Molecular Cell provides evidence that a translocating SWI/SNF-nucleosome complex efficiently displaces neighboring nucleosomes in vitro and may account for SWI/SNF-dependent nucleosome eviction in vivo.
PMCID: PMC3783944  PMID: 20513424
11.  Autophagy is impaired in cardiac ischemia-reperfusion injury 
Autophagy  2012;8(9):1394-1396.
Accumulating evidence attests to a prosurvival role for autophagy under stress, by facilitating removal of damaged proteins and organelles and recycling basic building blocks, which can be utilized for energy generation and targeted macromolecular synthesis to shore up cellular defenses. These observations are difficult to reconcile with the dichotomous prosurvival and death-inducing roles ascribed to macroautophagy in cardiac ischemia and reperfusion injury, respectively. A careful reexamination of ‘flux’ through the macroautophagy pathway reveals that autophagosome clearance is markedly impaired with reperfusion (reoxygenation) in cardiomyocytes following an ischemic (hypoxic) insult, resulting from reactive oxygen species (ROS)-mediated decline in LAMP2 and increase in BECN1 abundance. This results in impaired autophagy that is ‘ineffective’ in protecting against cell death with ischemia-reperfusion injury. Restoration of autophagosome clearance and by inference, ‘adequate’ autophagy, attenuates reoxygenation-induced cell death.
PMCID: PMC3442889  PMID: 22889942
BECN1; LAMP2; autophagic flux; cell death; ischemia-reperfusion; reactive oxygen species
12.  Proline dehydrogenase (oxidase), a mitochondrial tumor suppressor, and autophagy under the hypoxia microenvironment 
Autophagy  2012;8(9):1407-1409.
Proline dehydrogenase (oxidase, PRODH/POX), the first enzyme in the pathway of proline catabolism, has been identified as a mitochondrial, metabolic tumor suppressor, which is downregulated in a variety of human tumors. However, our recent findings show that PRODH/POX is upregulated by hypoxia in vitro and in vivo. The combination of low glucose and hypoxia produces additive effects on PRODH/POX expression. Both hypoxia and glucose depletion enhance PRODH/POX expression through AMP-activated protein kinase (AMPK) activation to promote tumor cell survival. Nevertheless, the mechanisms underlying PRODH/POX prosurvival functions are different for hypoxia and low-glucose conditions. Glucose depletion with or without hypoxia elevates PRODH/POX and proline utilization to supply ATP for cellular energy needs. Interestingly, under hypoxia PRODH/POX induces protective autophagy by generating reactive oxygen species (ROS). AMPK is the main initiator of stress-triggered autophagy. Thus, PRODH/POX acts as a downstream effector of AMPK in the activation of autophagy under hypoxia. This regulation was confirmed to be independent of the mechanistic target of rapamycin (MTOR) pathway, a major downstream target of AMPK signaling.
PMCID: PMC3442893  PMID: 22885468
apoptosis; autophagy; hypoxia; metabolic stress; proline dehydrogenase/oxidase
13.  The Growing Array of Innate Inflammatory Ignition Switches in Osteoarthritis 
Arthritis and rheumatism  2012;64(7):2055-2058.
Osteoarthritis (OA) is the most common form of arthritis and is a major cause of chronic pain and disability. We currently lack disease-modifying OA medical therapeutics that effectively slow or halt the progression to destruction and failure of articular cartilage. Importantly, OA is a disease of the whole joint, including not only meniscal fibrocartilage and hyaline articular cartilage, but also subchondral bone, periarticular musculature, tendons and ligaments, articular adipose tissue, synovium, and synovial fluid (SF). Clinically, varying degrees of synovitis and joint effusion in OA contribute to signs and symptoms of inflammation (1). Multiple lines of evidence suggest that OA progression is promoted by low-grade innate articular inflammation and by synovitis (1,2). “Conventional” inflammatory cytokines expressed in cartilage and synovium likely play a role, and interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), IL-6, IL-8, and IL-17 are among the players in synovitis (1,2). The report by Nair et al in this issue of Arthritis & Rheumatism reveals increased levels of soluble CD14 (sCD14) in SF to be a biomarker of innate inflammation in patients undergoing arthroscopic knee meniscectomy for treatment of meniscal tears (3). Investigators in this group previously characterized this population as “enriched for patients with preradiographic disease” (4), given the associated symptoms, synovitis, and evidence of articular cartilage damage detected by arthroscopy.
PMCID: PMC3711830  PMID: 22488656
14.  Rap1 and its regulatory proteins 
Small GTPases  2012;3(3):192-197.
Squamous cell carcinoma of the head and neck (SCCHN) is the sixth most common cancer, globally. Previously, we showed that Rap1GAP is a tumor suppressor gene that inhibits tumor growth, but promotes invasion in SCCHN. In this work, we discuss the role of Rap1 and Rap1GAP in SCCHN progression in the context of a microRNA-oncogene-tumor suppressor gene axis, and investigate the role of Rap1GAP in EZH2-mediated invasion. Loss of expression of microRNA-101 in SCCHN leads to upregulation of EZH2, a histone methyltransferase. Overexpression of EZH2 silences Rap1GAP via methylation, thereby promoting activation of its target, Rap1. This microRNA-controlled activation of Rap1, via EZH2-mediated silencing of Rap1GAP, is a novel mechanism of Rap1 regulation. In two independent SCCHN cell lines, downregulation of EZH2 inhibits proliferation and invasion. In both cell lines, stable knockdown of EZH2 (shEZH2) recovers Rap1GAP expression and inhibits proliferation. However, siRNA-mediated knockdown of Rap1GAP in these cells rescues proliferation but not invasion. Thus, EZH2 promotes proliferation and invasion via Rap1GAP-dependent and –independent mechanisms, respectively. Although the studies presented here are in the context of SCCHN, our results may have broader implications, given that Rap1GAP acts as a tumor suppressor in pancreatic cancer, thyroid cancer, and melanoma.
PMCID: PMC3442808  PMID: 22684501
EZH2; Rap1GAP; methylation; miR-101; translational
15.  E-box protein E2-2 is a crucial regulator of plasmacytoid DC development 
European journal of immunology  2008;38(9):2386-2388.
DC play central roles in priming both innate and adaptive immune responses. Multiple DC subsets have been identified on the basis of their phenotype and function. Plasmacytoid DC (pDC) are professional IFN-producing cells that play an essential role in anti-viral immunity. A series of recent studies demonstrates that the regulation of pDC development is different from other types of DC. In this issue of the European Journal of Immunology, new insight is provided into how human pDC development is regulated by various transcription factors, in particular by the Ets family protein Spi-B and E-box protein E2-2.
PMCID: PMC3652573  PMID: 18792016
DC; Developmental immunology; Transcription factors
16.  PI3K-Akt pathway regulates polycomb group protein and stem cell maintenance 
Cell Cycle  2013;12(2):199-200.
PMCID: PMC3575444  PMID: 23287474
PI3K; Akt; polycomb group protein; Bmi1; Ezh2; stem cell
17.  “Importin” signaling roles for import proteins 
Cell Adhesion & Migration  2012;6(1):4-12.
The formation of a mature myotendinous junction (MTJ) between a muscle and its site of attachment is a highly regulated process that involves myofiber migration, cell-cell signaling, and culminates with the stable adhesion between the adjacent muscle-tendon cells. Improper establishment or maintenance of muscle-tendon attachment sites results in a decrease in force generation during muscle contraction and progressive muscular dystrophies in vertebrate models. Many studies have demonstrated the important role of the integrins and integrin-associated proteins in the formation and maintenance of the MTJ. We recently demonstrated that moleskin (msk), the gene that encodes for Drosophila importin-7 (DIM-7), is required for the proper formation of muscle-tendon adhesion sites in the developing embryo. Further studies demonstrated an enrichment of DIM-7 to the ends of muscles where the muscles attach to their target tendon cells. Genetic analysis supports a model whereby msk is required in the muscle and signals via the secreted epidermal growth factor receptor (Egfr) ligand Vein to regulate tendon cell maturation. These data demonstrate a novel role for the canonical nuclear import protein DIM-7 in establishment of the MTJ.
PMCID: PMC3364137  PMID: 22647935
Drosophila Importin-7; Egfr signaling; Integrins; myogenesis; myotendinous junction; tendon cells
18.  Tipping the scales early: probing the long-term effects of obesity 
The Journal of Clinical Investigation  2012;122(11):3840-3842.
Obesity has reached epidemic proportions in the United States, and obesity-related illnesses have become a leading preventable cause of death. Childhood obesity is also growing in frequency, and the impact of a lifetime spent in the overweight state is only beginning to emerge in the literature. In this issue of the JCI, Bumaschny et al. used a genetic mouse model to investigate the self-perpetuating nature of obesity and shed some light on why it can become increasingly difficult to lose weight over time.
PMCID: PMC3484467  PMID: 23093788
19.  The impact of mitochondrial oxidative stress on bile acid-like molecules in C. elegans provides a new perspective on human metabolic diseases 
Worm  2013;2(1):e21457.
C. elegans is a model used to study cholesterol metabolism and the functions of its metabolites. Several studies have reported that, in worms, cholesterol is not a structural component of the membrane as it is in vertebrates. However, as in other animals, it is used for the synthesis of steroid hormones that regulate physiological processes such as dauer formation, molting and defecation. After cholesterol is taken up by the gut, mechanisms of transport of cholesterol between tissues in C. elegans involve lipoproteins, as in mammals. A recent study shows that both cholesterol uptake and lipoprotein metabolism in C. elegans are regulated by molecules whose activities, biosynthesis, and secretion strongly resemble those of mammalian bile acids, which are metabolites of cholesterol that act on metabolism in a variety of ways. Importantly, it was found that oxidative stress upsets the regulation of the synthesis of these molecules. Given the known function of mammalian bile acids as metabolic regulators of lipid and glucose homeostasis, future investigations of the biology of C. elegans bile acid-like molecules could provide information on the etiology of human metabolic disorders that are characterized by elevated oxidative stress.
PMCID: PMC3670457  PMID: 24058856
C. elegans; clk-1; bile acids; cholesterol; dafachronic acids; dauer formation; defecation; lipoproteins; metabolic syndrome; oxidative stress; steroid hormones
20.  Bioinformatic Challenges of Big Data in Non-Coding RNA Research 
Frontiers in Genetics  2012;3:178.
PMCID: PMC3438686  PMID: 22973302
21.  The THO/TREX complex functions in disease resistance in Arabidopsis 
Plant Signaling & Behavior  2012;7(3):422-424.
Powdery mildew pathogens are biotrophic fungi that infect large number of plant species. EDR1 (ENHANCED DISEASE RESISTANCE 1) is a negative regulator of plant disease resistance, and loss-of-function in the EDR1 gene confers enhanced disease resistance to powdery mildew pathogen Golovinomyces cichoracearum. In an edr1 suppressor screen, we recently found that a mutation in HPR1, a component of the THO/TREX complex, suppresses edr1-mediated disease resistance, however the hpr1 mutation enhances the ethylene-induced senescence in edr1. The hpr1 single mutant displays enhanced susceptibility, indicating that HPR1 is involved in plant defense responses.1 THO/TREX is a conserved protein complex that functions in pre-mRNA processing and mRNA export. Several components of THO/TREX complex in Arabidopsis have been identified. By searching Arabidopsis database, we found that Arabidopsis (Columbia-0) has two copies of UAP56, another component of the THO/TREX complex, and the UAP56 proteins are highly conserved. Similar to human UAP56 protein, Arabidopsis UAP56 also localizes to the nucleus, showing a pattern similar to the splicing speckles. Further characterization of the components of THO/TREX in Arabidopsis will provide new insights into the role of THO/TREX in defense responses in plants.
PMCID: PMC3443925  PMID: 22499202
HPR1; THO/TREX complex; UAP56; defense response; powdery mildew
22.  In vivo role of nitric oxide in plant response to abiotic and biotic stress 
Plant Signaling & Behavior  2012;7(3):437-439.
Over the past few years, nitric oxide (NO) has emerged as an important regulator in many physiological events, especially in response to abiotic and biotic stress. However, the roles of NO were mostly derived from pharmacological studies or the mutants impaired NO synthesis unspecifically. In our recent study, we highlighted a novel strategy by expressing the rat neuronal NO synthase (nNOS) in Arabidopsis to explore the in vivo role of NO. Our results suggested that plants were able to perform well in the constitutive presence of nNOS, and provided a new class of plant experimental system with specific in vivo NO release. Furthermore, our findings also confirmed that the in vivo NO is essential for most of environmental abiotic stresses and disease resistance against pathogen infection. Proper level of NO may be necessary and beneficial, not only in plant response to the environmental abiotic stress, but also to biotic stress.
PMCID: PMC3443929  PMID: 22499209
abiotic and biotic stress; disease resistance; drought; in vivo; nitric oxide; nitric oxide synthase; salinity
23.  Chromatin modification by SUMO-1 stimulates the promoters of translation machinery genes 
Nucleic Acids Research  2012;40(20):10172-10186.
SUMOylation of transcription factors and chromatin proteins is in many cases a negative mark that recruits factors that repress gene expression. In this study, we determined the occupancy of Small Ubiquitin-like MOdifier (SUMO)-1 on chromatin in HeLa cells by use of chromatin affinity purification coupled with next-generation sequencing. We found SUMO-1 localization on chromatin was dynamic throughout the cell cycle. Surprisingly, we observed that from G1 through late S phase, but not during mitosis, SUMO-1 marks the chromatin just upstream of the transcription start site on many of the most active housekeeping genes, including genes encoding translation factors and ribosomal subunit proteins. Moreover, we found that SUMO-1 distribution on promoters was correlated with H3K4me3, another general chromatin activation mark. Depletion of SUMO-1 resulted in downregulation of the genes that were marked by SUMO-1 at their promoters during interphase, supporting the concept that the marking of promoters by SUMO-1 is associated with transcriptional activation of genes involved in ribosome biosynthesis and in the protein translation process.
PMCID: PMC3488252  PMID: 22941651
24.  Promoters active in interphase are bookmarked during mitosis by ubiquitination 
Nucleic Acids Research  2012;40(20):10187-10202.
We analyzed modification of chromatin by ubiquitination in human cells and whether this mark changes through the cell cycle. HeLa cells were synchronized at different stages and regions of the genome with ubiquitinated chromatin were identified by affinity purification coupled with next-generation sequencing. During interphase, ubiquitin marked the chromatin on the transcribed regions of ∼70% of highly active genes and deposition of this mark was sensitive to transcriptional inhibition. Promoters of nearly half of the active genes were highly ubiquitinated specifically during mitosis. The ubiquitination at the coding regions in interphase but not at promoters during mitosis was enriched for ubH2B and dependent on the presence of RNF20. Ubiquitin labeling of both promoters during mitosis and transcribed regions during interphase, correlated with active histone marks H3K4me3 and H3K36me3 but not a repressive histone modification, H3K27me3. The high level of ubiquitination at the promoter chromatin during mitosis was transient and was removed within 2 h after the cells exited mitosis and entered the next cell cycle. These results reveal that the ubiquitination of promoter chromatin during mitosis is a bookmark identifying active genes during chromosomal condensation in mitosis, and we suggest that this process facilitates transcriptional reactivation post-mitosis.
PMCID: PMC3488253  PMID: 22941662
25.  Tubular actin filaments in tobacco guard cells 
Plant Signaling & Behavior  2011;6(10):1578-1580.
The dynamic remodeling of actin filaments in guard cells functions in stomatal movement regulation. In our previous study, we found that the stochastic dynamics of guard cell actin filaments play a role in chloroplast movement during stomatal movement. In our present study, we further found that tubular actin filaments were present in tobacco guard cells that express GFP-mouse talin; approximately 2.3 tubular structures per cell with a diameter and height in the range of 1–3 µm and 3–5 µm, respectively. Most of the tubular structures were found to be localized in the cytoplasm near the inner walls of the guard cells. Moreover, the tubular actin filaments altered their localization slowly in the guard cells of static stoma, but showed obvious remodeling, such as breakdown and re-formation, in moving guard cells. Tubular actin filaments were further found to be colocalized with the chloroplasts in guard cells, but their roles in stomatal movement regulation requires further investigation.
PMCID: PMC3256388  PMID: 21921692
actin dynamics; tubular actin filaments; chloroplast; guard cell; stomatal movement

Results 1-25 (57)