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PubMed2006

Relief of microRNA-mediated translational repression in human cells subjected to stress.

In metazoans, most microRNAs imperfectly base-pair with the 3' untranslated region (3'UTR) of target mRNAs and prevent protein accumulation by either repressing translation or inducing mRNA degradation. Examples of specific mRNAs undergoing microRNA-mediated repression are numerous, but whether the repression is a reversible process remains largely unknown. Here we show that cationic amino acid transporter 1 (CAT-1) mRNA and reporters bearing its 3'UTR can be relieved from the microRNA miR-122-induced inhibition in human hepatocarcinoma cells subjected to different stress conditions. The derepression of CAT-1 mRNA is accompanied by its release from cytoplasmic processing bodies and its recruitment to polysomes. The derepression requires binding of HuR, an AU-rich-element binding protein, to the 3'UTR of CAT-1 mRNA. We propose that proteins interacting with the 3'UTR will generally act as modifiers altering the potential of miRNAs to repress gene expression.

3' Untranslated Regions↗
PubMed2006

Targeting of aberrant mRNAs to cytoplasmic processing bodies.

In eukaryotes, a specialized pathway of mRNA degradation termed nonsense-mediated decay (NMD) functions in mRNA quality control by recognizing and degrading mRNAs with aberrant termination codons. We demonstrate that NMD in yeast targets premature termination codon (PTC)-containing mRNA to P-bodies. Upf1p is sufficient for targeting mRNAs to P-bodies, whereas Upf2p and Upf3p act, at least in part, downstream of P-body targeting to trigger decapping. The ATPase activity of Upf1p is required for NMD after the targeting of mRNAs to P-bodies. Moreover, Upf1p can target normal mRNAs to P-bodies but not promote their degradation. These observations lead us to propose a new model for NMD wherein two successive steps are used to distinguish normal and aberrant mRNAs.

Adaptor Proteins, Signal Transducing↗
PubMed2006

P-bodies react to stress and nonsense.

P-bodies are specialized cytoplasmic compartments where translational repression and mRNA turnover may occur. Findings in this issue of Cell provide evidence that P-bodies are sites of "mRNA purgatory." Bhattacharyya et al. (2006) reveal that normal mRNA can be released from P-bodies and translated into protein in response to stress. Meanwhile, Sheth and Parker (2006) report that aberrant mRNAs are targeted to P-bodies to undergo rapid decay.

3' Untranslated Regions↗
PubMed2005

Electrically induced gel-to-gel phase-transition in neurons.

At the end of transcardial perfusions with ice-cold physiological saline for 30 min or with isoosmotic potassium chloride for 5 min, but immediately before perfusion fixation, condenser-discharge electric shocks were administered to rats through surface electrodes pressed onto the temporal muscles of the scalped skull. As a result, striking ultrastructural compaction came about in numerous neurons thinly scattered in certain brain areas. Its features displayed a high degree of similarity to those previously observed following the in vivo administration of the same kind of electric shocks. This surprising independence from the actual state of metabolism questions whether the ultrastructural compaction, induced either in vivo or post mortem, is the result of any cascade of enzyme-mediated processes. On the other hand, a physical mechanism, phase transition propagated by non-covalent free energy stored in a cytoplasmic gel structure, which was proposed recently to explain a mechanically induced similar ultrastructural compaction, appears to apply also to the present case.

Animals↗
PubMed2005

A Place for RNAi.

Processing bodies (P bodies) are discrete cytoplasmic foci to which mRNA is routed for degradation. In mammalian cells, they are also associated with miRNA-induced translational silencing and siRNA-induced mRNA degradation. In a recent issue of Molecular Cell, Ding and coworkers described an argonaute-interacting protein that appears to promote the assembly of P bodies in C. elegans (Ding et al., 2005).

Animals↗
PubMed2005

The developmental timing regulator AIN-1 interacts with miRISCs and may target the argonaute protein ALG-1 to cytoplasmic P bodies in C. elegans.

In metazoans, microRNAs (miRNAs) carry out various regulatory functions through association with multiprotein miRNA-induced silencing complexes (miRISCs) that contain Dicer and Argonaute proteins. How miRNAs regulate the expression of their mRNA targets remains a major research question. We have identified the C. elegans ain-1 gene through a genetic suppressor screen and shown that it functions with the heterochronic genetic pathway that regulates developmental timing. Biochemical analysis indicates that AIN-1 interacts with protein complexes containing an Argonaute protein, Dicer, and miRNAs. AIN-1 shares homology with the candidate human neurological disease protein GW182, shown to localize in cytoplasmic processing bodies that are sites of mRNA degradation and storage. A functional AIN-1::GFP also localizes at the likely worm processing bodies. When coexpressed from transgenes, AIN-1 targets ALG-1 to the foci. These results suggest a model where AIN-1 regulates a subset of miRISCs by localization to the processing bodies, facilitating degradation or translational inhibition of mRNA targets.

Animals↗
PubMed2005

Myxoma of the renal capsule.

Myxomas are uncommon soft-tissue neoplasms, which are extremely rare in the kidney, with only five cases documented in the intraparenchymal location. However, renal capsular myxoma has not yet been reported. We describe a unique case of a clinically detected renal myxoma arising in the capsule. A 37-year-old man receiving treatment for epididymitis sought medical assistance for infertility. A radiological examination incidentally discovered a right renal tumor. The mass intruded into the perirenal tissue and measured 6 cm in major diameter. The resected kidney contained a well-circumscribed gelatinous capsular tumor. It was composed of sparse, bland, slender, spindle-shaped cells scattered in large amounts of basophilic interstitial mucoid material. The tumor cells showed diffuse immunoreactivity for vimentin. Occasional cells stained for alpha-smooth muscle actin and calponin. Reactivity was negative for S100 protein, epithelial membrane antigen, pancytokeratin, neurofilament protein, and h-caldesmon antibodies. Ultrastructural examination revealed fibroblast-like cells with long thin cytoplasmic processes, prominent rough endoplasmic reticulum, a well-developed Golgi complex, and secretory vesicles. No basal lamina was identified around the tumor cells. The differential diagnosis includes many other benign and malignant soft-tissue lesions exhibiting prominent secondary myxoid features. It is important to consider a renal capsular myxoma when examining lesions at this anatomic site to avoid misdiagnoses and to ensure that the patient receives appropriate treatment and prognostic information.

Adult↗
PubMed2007

Repression of protein synthesis by miRNAs: how many mechanisms?

MicroRNAs are approximately 21-nucleotide-long regulators of gene expression that gain access to their target mRNAs by complementary base pairing. Recent studies have revealed that animal microRNAs might take diverse routes to repress gene expression, affecting both target mRNA levels and translation. Mechanistic details of microRNA-mediated repression are starting to emerge but a comprehensive picture of the inhibition, and particularly the effects on mRNA translation, is still lacking. Recent data support different microRNA mechanisms and a role for cytoplasmic processing bodies in the degradation and storage of mRNAs targeted by microRNA regulators.

Animals↗
PubMed2005

Possible role of deep tubular invaginations of the plasma membrane in MHC-I trafficking.

Tubules and vesicles are membrane carriers involved in traffic along the endocytic and secretory routes. The small GTPase Arf6 regulates a recycling branch of short dynamic tubular intermediates used by major histocompatibility class I (MHC-I) molecules to traffic through vesicles between endosomes and the plasma membrane. We observed that Arf6 also affects a second network of very long and stable tubules containing MHC-I, many of which correspond to deep invaginations of the plasma membrane. Treatment with wortmannin, an inhibitor of phosphatidylinositol-3-phosphate kinase, prevents formation of the short dynamic tubules while increasing the number of the long and very stable ones. Expression of NefAAAA, a mutant form of HIV Nef, increases the number of cells containing the stable tubules, and is used here as a tool to facilitate their study. Photoactivation of NefAAAA-PA-GFP demonstrates that this molecule traffics from endosomes to the tubules. Finally, live-cell imaging also shows internalization of MHC-I molecules into these tubules, suggesting that this is an additional route for MHC-I traffic.

ADP-Ribosylation Factor 6↗
PubMed2003

Distinct roles of Rab3B and Rab13 in the polarized transport of apical, basolateral, and tight junctional membrane proteins to the plasma membrane.

Regulated transport of proteins to distinct plasma membrane domains is essential for the establishment and maintenance of cell polarity in all eukaryotic cells. The Rab family small G proteins play a crucial role in determining the specificity of vesicular transport pathways. Rab3B and Rab13 localize to tight junction in polarized epithelial cells and cytoplasmic vesicular structures in non-polarized fibroblasts, but their functions are poorly understood. Here we examined their roles in regulating the cell-surface transport of apical p75 neurotrophin receptor (p75NTR), basolateral low-density lipoprotein receptor (LDLR), and tight junctional Claudin-1 using transport assay in non-polarized fibroblasts. Overexpression of Rab3B mutants inhibited the cell-surface transport of LDLR, but not p75NTR and Claudin-1. In contrast, overexpression of Rab13 mutants impaired the transport of Claudin-1, but not LDLR and p75NTR. These results suggest that Rab3B and Rab13 direct the cell-surface transport of LDLR and Claudin-1, respectively, and may contribute to epithelial polarization.

Animals↗
PubMed2003

Sublethal effects of phenol on spermatogenesis in sea urchins (Anthocidaris crassispina).

Adult sea urchins, Anthocidaris crassispina, were exposed to 0.1 and 10 mgL(-1) phenol for 4 weeks. Abnormal sperm development was clearly evident in phenol-treated sea urchins, although no mortality was found throughout the exposure period. Occurrences of multinucleate sperm cells (including spermatocytes to spermatozoa) showed a significant increase from 0.07% in the control to 10.7% and 43.3% in the 0.1- and 10-mgL(-1) treatments, respectively (P<0.01). Likewise, sperm with electron dense, dark tails increased significantly from 8% in the control to 36.6% and 43.4% in the 0.1- and 10-mgL(-1) phenol-treated sea urchins, respectively (P<0.01). In addition, disruption of cytoplasmic membranous structures such as loss of mitochondrial cristae and distortion of mitochondrial membranes and nucleus envelope were commonly found in phenol-treated spermatogonia and spermatocytes. Previous studies have clearly demonstrated motility impairment and a concomitant reduction of fertilization capability in sea urchin sperm with dark tails and/or distorted mitochondria. Our current findings therefore suggest that chronic exposure to phenol at 0.1 mgL(-1) could lower the quality of sperm and reproductive success in sea urchins, which may threaten the survival of these ecologically important species. The observed impairment of spermatogenesis by phenol might also occur in other invertebrate species.

Animals↗
PubMed2003

Interaction of Sedlin with chloride intracellular channel proteins.

Sedlin is an evolutionarily conserved protein encoded by the causative gene SEDL for spondyloepiphyseal dysplasia tarda. Nevertheless, how Sedlin mutations cause the disease remains unknown. Here, the intracellular chloride channel protein CLIC1 was shown to associate with Sedlin by yeast two-hybrid screening. Green fluorescence protein-CLIC1 readily co-immunoprecipitated with FLAG-Sedlin. In addition, both proteins colocalized extensively in cytoplasmic vesicular/reticular structures in COS-7 cells, suggesting their interaction at intracellular membranous organelles. Sedlin also associated with CLIC2 in yeast two-hybrid assays. The link between Sedlin and the intracellular chloride channels is the first step to understand their functional interplays.

Animals↗
PubMed2004

The role of neurotransmission and the Chopper domain in p75 neurotrophin receptor death signaling.

The role of p75 neurotrophin receptor (p75NTR) in mediating cell death is now well characterized, however, it is only recently that details of the death signaling pathway have become clearer. This review focuses on the importance of the juxtamembrane Chopper domain region of p75NTR in this process. Evidence supporting the involvement of K+ efflux, the apoptosome (caspase-9, apoptosis activating factor-1, APAF-1, and Bcl-xL), caspase-3, c-jun kinase, and p53 in the p75NTR cell death pathway is discussed and regulatory roles for the p75NTR ectodomain and death domain are proposed. The role of synaptic activity is also discussed, in particular the importance of neutrotransmitter-activated K+ channels acting as the gatekeepers of cell survival decisions during development and in neurodegenerative conditions.

Animals↗
PubMed1986

The spectrum of liver disease in the acquired immunodeficiency syndrome.

Abnormal liver chemistries, unexplained fevers, or hepatomegaly prompted 36 liver biopsies on 34 patients with the acquired immunodeficiency syndrome. The most common finding was the presence of hepatic granulomas, seen in 13 of the biopsy specimens. Eight of these granulomas were ill-defined, and 5 were more clearly associated with mycobacterial disease. Portal fibrosis and fatty infiltration were common, but a paucity of significant inflammatory activity was seen despite elevated aspartate aminotransferase levels, perhaps related to the underlying immunoincompetent status. Other noteworthy histopathologic findings included 1 patient each with peliosis hepatis and cryptococcal hepatitis. Electron-microscopic evidence of cytoplasmic tubular structures or viral particles were seen within the hepatocytes of 2 patients. It is concluded that a broad spectrum of hepatic histopathology may be seen in the acquired immunodeficiency syndrome, and that liver biopsy may be diagnostically valuable in the clinical investigation of such patients.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Renal and hepatic angiomyolipomas in a child without evidence of tuberous sclerosis.

A renal neoplasia, displaying the typical features of angiomyolipoma (an admixture of smooth muscle cells, mature adipocytes and tangles of thick-walled blood vessels) was found in a nine-year-old boy. In addition, cytoplasmic crystalloid structures and HMB 45 positivity were found in smooth muscle cells. Similar findings were also observed in a small nodule of the liver. According to literature data, angiomyolipoma is very rare in children and almost exclusively associated with tuberous sclerosis. Our case suggest that the diagnostic hypothesis of angiomyolipoma can not be disregarded when a renal mass is identified in a young patient even in a clinical setting other than tuberous sclerosis.

Angiomyolipoma↗
PubMed1992

Primary phase of hepatocytic autophagocytosis under ischaemic conditions.

Increased autophagocytosis in hepatocytes was found in response to conditions of ischaemia/hypoxia. Initial stages proved to be recordable. These were found to become manifest through the formation of phospholipid membrane structures, approximately 5 nm in width, coalescing in circular formations with vesicular extensions. They may further develop to form multilayer myelin structures. Enveloped cytoplasmic regions and organelles were unchanged, at the beginning, and subsequently coalesced typically into autophagolysosomes and autophagic vacuoles. Verification will be necessary to find out if these initial stages occur only in response to hypoxia or constitute a phenomenon of general validity.

Animals↗