Role of MAP1B in axonal retrograde transport of mitochondria

The MAPs (microtubule-associated proteins) MAP1B and tau are well known for binding to microtubules and stabilizing these structures. An additional role for MAPs has emerged recently where they appear to participate in the regulation of transport of cargos on the microtubules found in axons. In this role, tau has been associated with the regulation of anterograde axonal transport. We now report that MAP1B is associated with the regulation of retrograde axonal transport of mitochondria. This finding potentially provides precise control of axonal transport by MAPs at several levels: controlling the anterograde or retrograde direction of transport depending on the type of MAP involved, controlling the speed of transport and controlling the stability of the microtubule tracks upon which transport occurs.     

Bacterial endotoxin and tumor necrosis factor stimulate prostaglandin production by human decidua

The purpose of these studies was to determine the effect of bacterial endotoxin and tumor necrosis factor (TNF) on prostaglandin (PG) secretion by human decidua. Decidual explants were established from women undergoing elective cesarean sections before the onset of labor. Escherichia Coli endotoxin and purified human recombinant TNF (rh TNF) were incubated with decidual explants. PGF2 alpha and PGE2 biosynthesis was measured by radioimmunoassay. A significant increase in the release of all PGs into the media occurred in response to LPS and TNF. In the setting of an extraamniotic infection, bacterial and host secretory products (TNF) could trigger the onset of labor, activating the decidua to produce PGs.     

Tau regulates the localization and function of End‐binding proteins 1 and 3 in developing neuronal cells

The axonal microtubule‐associated protein tau is a well‐known regulator of microtubule stability in neurons. However, the putative interplay between tau and End‐binding proteins 1 and 3 (EB1/3), the core microtubule plus‐end tracking proteins, has not been elucidated yet. Here, we show that a cross‐talk between tau and EB1/3 exists in developing neuronal cells. Tau and EBs partially colocalize at extending neurites of N1E‐115 neuroblastoma cells and axons of primary hippocampal neurons, as shown by confocal immunofluorescence analyses. Tau down‐regulation leads to a reduction of EB1/3 comet length, as observed in shRNA‐stably depleted neuroblastoma cells and TAU?/? neurons. EB1/3 localization depends on the expression levels and localization of tau protein. Over‐expression of tau at high levels induces EBs relocalization to microtubule bundles at extending neurites of N1E‐115 cells. In differentiating primary neurons, tau is required for the proper accumulation of EBs at stretches of microtubule bundles at the medial and distal regions of the axon. Tau interacts with EB proteins, as shown by immunoprecipitation in different non‐neuronal and neuronal cells and in whole brain lysates. A tau/EB1 direct interaction was corroborated by in vitro pull‐down assays. Fluorescence recovery after photobleaching assays performed in neuroblastoma cells confirmed that tau modulates EB3 cellular mobility. In summary, we provide evidence of a new function of tau as a direct regulator of EB proteins in developing neuronal cells. This cross‐talk between a classical microtubule‐associated protein and a core microtubule plus‐end tracking protein may contribute to the fine‐tuned regulation of microtubule dynamics and stability during neuronal differentiation.

     

Phylogeographic history of Patagonian lizards of the Liolaemus elongatus complex (Iguania: Liolaemini) based on mitochondrial and nuclear DNA sequences

In this study, we present a phylogeographic analysis of a group of lizards distributed in north‐western Patagonia, the Liolaemus elongatus complex. We sequenced 581 individuals for one mitochondrial gene (cytochrome‐b), and for a subset, we sequenced another mitochondrial gene (12S rRNA) and two nuclear genes: kinesin family member 24 (KIF24) and the anonymous nuclear locus LDAB1D. We estimated gene trees, mitochondrial and nuclear haploytpe networks, standard molecular diversity indices, genetic distances between lineages and Bayesian skyline plots. Our results provide evidence for recognition of seven species previously described within the L. elongatus complex: Liolaemus antumalguen, Liolaemus chillanensis, Liolaemus carlosgarini, Liolaemus burmeisteri, Liolaemus smaug, Liolaemus elongatus and Liolaemus crandalli, but we did not find sufficient evidence to support Liolaemus choique, Liolaemus shitan or Liolaemus sp. 6 as distinct species. We identified four candidate species (Liolaemus sp. 1, Liolaemus sp. 2, Liolaemus sp. 3 and Liolaemus sp. 7), and we discuss evolutionary processes that may have contributed to the origin of these lineages and their taxonomic and conservation implications.     

Variations in the cytoplasmic region account for the heterogeneity of the chicken MHC class I (B-F) molecules

Molecular variation among major histocompatibility complex (MHC) class I (B-F) proteins from B-homozygous chickens is apparently caused by C-terminal variation. Analysis of the total B-F protein pool revealed substantial heterogeneity with two or three molecular mass constituents, each being comprised by several isoelectric focusing variants. This heterogeneity could not be reduced by enzymatic deglycosylation. By contrast, proteolytic removal of a small (M _r 1000–4000) fragment from the chain resulted in the generation of a M _r 36 000 fragment, common to all the molecular mass variants. Unlike the parent proteins, the M _r 36 000 fragment derived from isolated variants yielded identical, simple patterns in two-dimensional gel electrophoresis and identical finger prints in peptide mapping. This, together with N-terminal amino acid sequencing, as well as comparison of hydrophobicity properties of fragments obtained by gradual proteolytic digestion, indicated that the small peptide responsible for the major B-F heterogeneity was situated in the intracellular, C-terminal part.     

Glycosaminoglycans and beta-amyloid,prion and tau peptides in neurodegenerative diseases

Protein aggregation into dense filamentous inclusions is a characteristic feature of many etiologically diverse neurodegenerative disorders including Alzheimer's disease (AD), spongiform encephalopathies, and tauopathies. Thus, beta-amyloid peptide (Abeta) accumulates within senile amyloid plaques in AD, protease-resistant prion protein constitutes the amyloid deposits in spongiform encephalopathies and tau protein gives rise to neurofibrillary tangles (NFT) both in AD and in tauopathies. Curiously, these abnormal protein inclusions contain, in addition to their major peptide components, some associated sulfated glycosaminoglycans (sGAG). Here we discuss the proposal that the binding of sGAG to aggregate-forming peptides may modify the pathogenic process depending on their subcellular localization.     

Microtubule-associated protein 1B (MAP1B) is required for dendritic spine development and synaptic maturation

Microtubule-associated protein 1B (MAP1B) is prominently expressed during early stages of neuronal development, and it has been implicated in axonal growth and guidance. MAP1B expression is also found in the adult brain in areas of significant synaptic plasticity. Here, we demonstrate that MAP1B is present in dendritic spines, and we describe a decrease in the density of mature dendritic spines in neurons of MAP1B-deficient mice that was accompanied by an increase in the number of immature filopodia-like protrusions. Although these neurons exhibited normal passive membrane properties and action potential firing, AMPA receptor-mediated synaptic currents were significantly diminished. Moreover, we observed a significant decrease in Rac1 activity and an increase in RhoA activity in the post-synaptic densities of adult MAP1B(+/-) mice when compared with wild type controls. MAP1B(+/-) fractions also exhibited a decrease in phosphorylated cofilin. Taken together, these results indicate a new and important role for MAP1B in the formation and maturation of dendritic spines, possibly through the regulation of the actin cytoskeleton. This activity of MAP1B could contribute to the regulation of synaptic activity and plasticity in the adult brain.     

Biological basis for the management of ‘lugs negra’ (Sarcothalia crispata Gigartinales,Rhodophyta) in southern Chile

The present paper describes growth dynamics in a natural bed of the resource luga negra (Sarcothalia crispata) in Guapilinao, southern Chile (41°57 S, 73°31 W). This resource is currently harvested and exported as raw material for the production of carrageenan. Seasonal variation in biomass, frond size, density and phenology was determined by periodic sampling. Natural recruitment was evaluated on different substrata added to the field; at the same time, substrata were inoculated under greenhouse conditions. Results showed that luga negra has seasonal growth: biomass increased from a minimum in spring to a maximum in mid to late summer. On the other hand, density was minimal in winter (200 ind. m^–2) and increased to 2000 ind. m^–2 in late spring. Peak abundance of mature tetrasporic fronds occurred in late summer, whereas that of cystocarpic fronds occurred in winter. Recruitment began in summer and extended into winter. Survival on different substrata were compared. Gametophytes had better survival rates on clam shells and 5 mm rope while tetrasporophytes had the best survival rate on clam shells and secondarily on boulders.