Enhanced acetylation of alpha-tubulin in influenza A virus infected epithelial cells

Husain, Matloob; Harrod, Kevin S.

doi:10.1016/j.febslet.2010.11.023

Cited by 71 publications

(73 citation statements)

References 20 publications

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“…We have shown here the up-regulation of EsTUBA in hepatopancreas after V. parahaemolyticus challenge was consistent with previous studies in other genes such as the upregulation of Hsp70 in swimming crab challenged by V. alginolyticus [46] and the up-regulation of EsCTL in hepatopanceras of E. sinensis challenged by V. parahaemolyticus [21]. In addition, the previous study has shown the enhancement in the level of α-tubulin in influenza A virus-infected cells [47]. Hepatopancreas, gill and intestine are important organs involved in crustacean immunities, and play a crucial role in the immune response [48].…”

Section: Discussionsupporting

confidence: 80%

Identification of an Alpha-Tubulin Gene from the Chinese Mitten Crab Eriocheir sinensis: Expression Profiles under Immune Challenge and during Larval Development

Jiang¹,

Sun²,

Lin³

et al. 2015

J Biotechnol Biomater

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In this study, an alpha-tubulin gene (EsTUBA, GenBank: KJ509188) was isolated and identified from the Chinese mitten crab Eriocheir sinensis. The EsTUBA mRNA expression patterns under larval brachyurization development and immune challenge stress by Vibrio parahaemolyticus injection in adult crabs were evaluated. EsTUBA cDNA was 1,695 base pairs (bp) with an open-reading frame of 1,356 bp encoding 451 amino acids (49.95 kDa) and containing GTPase domain and C-terminal Tubulin domain. Sequence alignment showed that EsTUBA shared 95-98% identity and exactly similar structural features with its counterparts reported in other animals. Phylogenetic analysis indicated that EsTUBA clustered into one group together with Tubulins from other crustaceans. Sequence alignment, structure comparison and bioinformatic analyses revealed that EsTUBA is member of the Tubulin family. EsTUBA was fluctuant expressed in all tested larval development stages and various organs, and the levels of EsTUBA mRNA expressed in hepatopancreas, gill and intestine, are significantly expression fluctuated and induced after bacteria V. parahaemolyticus injection, while in heart, is almost consistently expressed at 0, 6, 12, 24, 36 and 48 h post-injection compared to control. The molecular cloning of EsTUBA gene is important for further study on the function of this gene.

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Section: Discussionsupporting

confidence: 80%

Identification of an Alpha-Tubulin Gene from the Chinese Mitten Crab Eriocheir sinensis: Expression Profiles under Immune Challenge and during Larval Development

Jiang¹,

Sun²,

Lin³

et al. 2015

J Biotechnol Biomater

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“…113 RhoA, on the other hand, is involved in downregulation of HDAC6 activity, leading to increased microtubule acetylation, which in turn is associated with enhanced virus assembly and release. 114 In recent years, PAK1 was reported to contribute to ERK phosphorylation and thereby enhance influenza virus production, although the mechanism involved remained elusive. 115,116 Another publication also reported ERK activation upon influenza infection, but showed that this was mediated by RhoA.…”

Section: Virus Assembly and Egressmentioning

confidence: 99%

Rho’ing in and out of cells

2014

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These authors contributed equally to this work Keywords: Rho GTPase, actin, egress, entry, gene expression, immune system, transformation, virus Rho GTPases are key regulators of actin and microtubule dynamics and organization. increasing evidence shows that many viruses have evolved diverse interactions with Rho GTPase signaling and manipulate them for their own benefit. in this review, we discuss how Rho GTPase signaling interferes with many steps in the viral replication cycle, especially entry, replication, and spread. Seen the diversity between viruses, it is not surprising that there is considerable variability in viral interactions with Rho GTPase signaling. However, several largely common effects on Rho GTPases and actin architecture and microtubule dynamics have been reported. For some of these processes, the molecular signaling and biological consequences are well documented while for others we just begin to understand them. A better knowledge and identification of common threads in the different viral interactions with Rho GTPase signaling and their ultimate consequences for virus and host may pave the way toward the development of new antiviral drugs that may target different viruses.©2014 Landes Bioscience. Do not distribute. e28318-2Small GTPases volume 5effector of ROCK, which phosphorylates and inhibits cofilin.14 Cofilin is an F-actin-severing protein. Mainly depending on the local availability of G-actin monomers, cofilin activity may lead to net actin depolymerization or increased actin polymerization and branching. Other RhoA effectors include members of the ezrin/radixin/moesin (ERM) proteins 15 . Rac1 is thought to release WAVE from an inhibited complex, thereby activating the actin-polymerizing complex Arp2/3. 16,17 Active Arp2/3 mediates branching and elongation of existing actin filaments, generating a meshwork. Cdc42 also activates Arp2/3 through a direct interaction with the Arp2/3 activators Wiskott-Aldrich syndrome protein (WASP) or N-WASP.18 Both Rac1 and Cdc42 also activate group I serine/threonine p21 activating kinases (PAK). These different signalization branches are interconnected. In general, RhoA pathway signaling counteracts the Rac1 and Cdc42 signaling axes and vice versa.Because Rho GTPase signaling is involved in a plethora of cellular processes, it is perhaps not surprising that several viral gene products have evolved to interfere with and modulate these signaling axes. Indeed, several viruses interfere with the actin cytoskeleton and Rho GTPase signaling during many steps of their replication cycle. During entry and egress, these interactions may allow or facilitate viral particle passage across the cortical actin barrier and to rearrange actin to conformations that promote virus infection and spread, while other viral processes, such as intracellular movement, gene expression and latency, but also interaction with the immune system or oncogenesis may also depend to some extent on Rho GTPase signaling and associated actin rearrangements. In this review, the current kno...

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“…At least eight viruses, including six DNA viruses, induce tubulin acetylation to varying extents, and in some cases, evidence suggests that stable MTs may be important for infection (5)(6)(7)(8)(9)(10)(11)(12)(13)(14). However, the underlying mechanisms by which many viruses remodel host MT networks and potential roles for +TIPs remain poorly understood.…”

mentioning

confidence: 99%

Plus-end tracking proteins, CLASPs, and a viral Akt mimic regulate herpesvirus-induced stable microtubule formation and virus spread

Naghavi

Gundersen

Walsh

2013

Proc. Natl. Acad. Sci. U.S.A.

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Although microtubules (MTs) frequently form highly dynamic networks, subsets of MTs become stabilized in response to environmental cues and function as specialized tracks for vesicle and macromolecular trafficking. MT stabilization is controlled by specialized plus-end tracking proteins (+TIPs) whose accumulation at the MT ends is facilitated by the end-binding protein, EB1, and regulated by various signaling pathways. As cargoes themselves, viruses are dependent on MTs for their intracellular movement. Although many viruses affect MT organization, the potential contribution of MT stabilization by +TIPs to infection remains unknown. Here we show that early in infection of primary human fibroblasts, herpes simplex virus type 1 (HSV-1) disrupts the centrosome, the primary MT organizing center in many cell types. As infection progresses HSV-1 induces the formation of stable MT subsets through inactivation of glycogen synthase kinase 3beta by the viral Ser/Thr kinase, Us3. Stable MT formation is reduced in cells infected with Us3 mutants and those stable MTs that form cluster around the trans-Golgi network. Downstream of glycogen synthase kinase 3beta, cytoplasmic linker-associated proteins (CLASPs), specialized host +TIPs that control MT formation at the trans-Golgi network and cortical capture, are specifically required for virus-induced MT stabilization and HSV-1 spread. Our findings demonstrate the biological importance of +TIPs to viral infection and suggest that HSV-1 has evolved to exploit the trans-Golgi network as an alternate MT organizing center to facilitate virus spread.M icrotubules (MTs) function in a variety of processes, including directed intracellular trafficking of cargos and changes in cell shape, polarity, and motility (1, 2). Consisting of polarized heteropolymers of α/β-tubulin, in most cells MT minusends are anchored at the perinuclear MT organizing center (MTOC), whereas their plus-ends radiate toward the cell periphery. In proliferating cells, the majority of MTs are highly dynamic, growing and shrinking through the addition or loss of tubulin subunits primarily at the plus-end. Dynamic instability facilitates intracellular sensing through "search-and-capture." On encountering targets such as the cell cortex and in response to specific signals, subsets of MTs become stabilized and acquire posttranslational modifications such as acetylation and detyrosination (3). Stable MTs are recognized by specific motor proteins and act as specialized tracks for vesicle transport (1, 3). MT stabilization is mediated by proteins that track dynamic MT plusends and influence rates of MT growth, pause, and collapse, known as plus-end tracking proteins (+TIPs) (4). Central to plusend tracking is EB1, a member of the end-binding family of proteins that recognizes growing MT ends. Although many +TIPs are capable of associating with MTs, it is their interaction with EB1 that mediates their specific accumulation at MT plus-ends (4). +TIP activity and interaction with EB1 responds to signals including Rho-Dia act...

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Enhanced acetylation of alpha-tubulin in influenza A virus infected epithelial cells

Cited by 71 publications

References 20 publications

Identification of an Alpha-Tubulin Gene from the Chinese Mitten Crab Eriocheir sinensis: Expression Profiles under Immune Challenge and during Larval Development

Identification of an Alpha-Tubulin Gene from the Chinese Mitten Crab Eriocheir sinensis: Expression Profiles under Immune Challenge and during Larval Development

Rho’ing in and out of cells

Plus-end tracking proteins, CLASPs, and a viral Akt mimic regulate herpesvirus-induced stable microtubule formation and virus spread

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