Function Of L1 Research Articles

Ethanol Does Not Inhibit the Adhesive Activity ofDrosophila Neuroglian or Human L1 in DrosophilaS2 Tissue Culture Cells

Members of the L1 family of homophilic neural cell adhesion molecules are thought to play an important role in nervous system development and function. It is also suggested that L1 is a direct target of ethanol in fetal alcohol syndrome, since ethanol inhibits the aggregation of cultured cells expressing L1 (Ramanathan, R., Wilkemeyer, M. F., Mittel, B., Perides, G., and Charness, M. E. (1996) J. Cell Biol. 133, 381-390). If ethanol acts directly on the homophilic adhesive function of the L1 molecule, then inhibition of aggregation by ethanol should be observed in any cell type that expresses L1. Here we examined the effect of physiologically relevant concentrations of ethanol on the aggregation of Drosophila S2 cells that expressed either neuroglian (the Drosophila homolog of L1) or human L1. The aggregation of these S2 cells is known to be solely dependent on the homophilic interactions between L1 or neuroglian molecules. Neither cell adhesion molecule was affected when cell aggregation assays were carried out in the presence of >/=38 mM ethanol. The recruitment of membrane skeleton assembly at sites of cell-cell contact (a transmembrane signaling function of human L1) was also unaffected by the presence of ethanol. Thus the previously described inhibition of cell adhesion by ethanol in L1-expressing cells cannot be explained by a simple direct effect on the adhesive activity of L1 family members.

Hund's rules

We review the present state of our undertanding of Hund's first and second rules, their domains of validity, and of generalizations in cases where the rules in their original form are invalid. These exceptions occur mainly in atomic configurations with more than one open shell withl ≥ 1, but also in cases with large orbital angular momentaL. We present a derivation of thealternating rule, which is, in some sense, a generalization of Hund's first rule, and present new rules, which generalize Hund's second rule. The importance of the concept ofunnatural parity states for an understanding of these rules is stressed. It is demonstrated that the lowest singlet-triplet average energy for the sameL corresponds to a pair of unnatural parity states (theunnatural parity rule). For sufficiently smalll 1 andl 2, the lowest average energy is that of the pair of states with the maximum possibleL (maximum-L rule), though exceptions are found already for moderately large values ofl 1 andl 2. Our analysis indicates that the validity of Hund's second rule is to some extent an accidental consequence of the minimisation of an elementary function ofl 1,l 2, andL — which does not depend monotonically onL — over states of unnatural parity, and that a more general and more fundamental rule should be formulated in terms of this function. We also discuss the generalisation of Hund's rules to molecules, as well as violations of them, with particular emphasis on the inversion of Hund's first rule by spin-polarization in molecules.

Involvement of lysine 270 and lysine 271 of yeast 5S rRNA binding protein in RNA binding and ribosome assembly

Contributions of the highly conserved K270 and its neighboring K271 in the C-terminal region of the yeast ribosomal protein L1 to 5S rRNA binding and ribosome assembly were examined by in vivo and in vitro studies on the consequences of 14 substitution mutations. All mutant proteins with a single amino-acid substitution at either position were able to bind 5S rRNA in vitro to an extent comparable to the wild-type. Yeast cells expressing these mutant proteins, except the K270G mutant, grew at nearly normal rates. Mutations of K270 appeared to produce more demonstrable effects than those of K271. The double mutant K270,271G bound RNA poorly and yeast cells expressing the mutant protein grew 30% slower. Double mutants K270,271E and K270,271R were lethal, although the mutant protein was assembled into the 60S ribosomal subunits. The resultant subunits were not stable leading eventually to cell death. The in vitro RNA binding ability of the respective protein was reduced by 60% and 20%. Taken together, the present data identified K270 and K271 as important amino-acid residues in the function of the yeast ribosomal protein L1.

Expression and function of the neural cell adhesion molecule L1 in mouse leukocytes.

The neural cell adhesion molecule L1 is a cell surface glycoprotein of the immunoglobulin superfamily which mediates adhesion between neural cells. The possibility that similar cell-cell recognition mechanisms may be shared by the nervous and immune systems prompted us to study the expression and function of L1 in cells of the hematopoietic system. Immunofluorescence analysis using monoclonal L1 antibody revealed that the molecule is expressed in the bone marrow, spleen, and thymus of the mouse. This observation was confirmed by amplifying cDNA derived from these organs by the polymerase chain reaction with L1-specific oligonucleotide primers. Two-color fluorescence analysis indicated that bone marrow lymphoid and granulocyte precursor cells express low and high levels of L1, respectively. In the thymus L1 is primarily expressed by mature cells that have a strong expression of CD3 and in the spleen both B cells and T cells express L1. The possible function of L1 in lymphoid cells was studied using subcloned ESb-MP lymphoma cells having high or low densities of L1 on the cell surface as well as activated splenic B lymphoblasts. Parental and subcloned ESb-MP cells that strongly expressed L1 could form homotypic aggregates in the presence of low Ca2+ levels, whereas subcloned ESb-MP cells with a weak expression of L1 did not aggregate, suggesting that L1 mediates the Ca(2+)-independent aggregation of the parental ESb-MP cells. Furthermore, the aggregation of activated B lymphoblasts under physiological concentrations of Ca2+ and Mg2+ was inhibited by 30% in the presence of Fab fragments of polyclonal L1 antibodies, implying that L1 also mediates adhesion among normal lymphoid cells. A possible role of L1 on lymphocytes in stimulating the innervation of lymphoid organs is discussed.

Functional expression of a full-length cDNA coding for rat neural cell adhesion molecule L1 mediates homophilic intercellular adhesion and migration of cerebellar neurons.

Neural cell adhesion molecule L1 is postulated to be involved in cell-cell interaction, neurite elongation, fasciculation of axons, cell migration, and myelination. To determine the function of L1 directly, we have transfected rat L1 cDNA into mouse fibroblast L cells. Stable transformants expressing L1 showed uniform surface expression of the molecule without phenotypic changes. Dispersed L1-expressing transfectants aggregated with faster kinetics than control cells in a homophilic manner. Divalent cations were not required for this cell aggregation. L1-transfected cells markedly enhanced neuronal cell adhesion and migration in co-culture with rat cerebellar neurons. These results indicate that L1 is involved in a determinant step of neural development through molecular interactions.

Molecular cloning of cDNA encoding the rat neural cell adhesion molecule L1 Two L1 isoforms in the cytoplasmic region are produced by differential splicing

We have isolated and sequenced a full-length cDNA encoding the rat neural cell adhesion molecule L1. The deduced amino acid sequence as a whole shows high homology to mouse L1 sequence. In addition to this complete form of L1, we found an isoform, L1cs, which lacks four animo acid residues (RSLE) in the cytoplasmic domain and probably is derived from the same single L1 gene by tissue-specific alternative splicing. While L1 mRNA was predominantly expressed in the brain, L1cs mRNA was found exclusively in peripheral nervous tissue. Differential splicing in the highly conserved cytoplasmic domain may play an important role in modulating the function of L1 in different cells.

Listening Perception Accuracy of ESL Learners as a Variable Function of Speaker L1

U As we incorporate into our ESL speaking classes a greater number of interactive tasks involving nonnative-speaker/nonnative-speaker (NNS/ NNS) dyads or groups, trying to create the optimum conditions for learners to benefit from negotiated input (Long, 1983; Doughty & Pica, 1986), we have tended to move away from exercises that focus on linguistic form, particularly in terms of the pronunciation and perception of English sound contrasts at the syllable or word level. This would seem to be justified if we could be sure that, as an inevitable part of receiving negotiated input, learners were in fact developing sufficient accuracy in the production and perception of those features of spoken English that play a crucial part in comprehension. According to Long and Porter (1985), accuracy does not suffer when learners take part in interactive pair work with other NNSs. However, this claim was primarily based on the use of grammatical structures and seems, in our experience, to be less tenable when we think of some learners whose accuracy in spoken production does seem to be subject to some variation. We do not know of any studies focusing specifically on level of pronunciation and perception accuracy in NNS/NNS pair work, but we have observed that learners seem to get by with fairly inaccurate pronunciations (in terms of the target) when their NNS partner is very familiar with their speech, particularly in the EFL context where interlocutors share the same L1 (Kenworthy, 1987). We wondered if ESL learners actually found it easier to identify English words when these were spoken by other learners than when they were spoken by English native speakers. In an attempt to answer this question, we designed a listening perception exercise to investigate whether learners became more or less accurate in their identification of English words as a function of the Li of the speaker.

Characterization of the biosynthesis, membrane association and function of the cell adhesion molecule L1

The L1 cell adhesion molecule is involved in cell migration and cell-cell adhesion in the brain. In this report we describe a purification procedure which allowed simultaneous isolation of L1 and the neural cell adhesion molecule. Furthermore, we studied L1 biosynthesis, post-translational modifications and function. L1 was synthesized as a polypeptide with relative molecular weight 200,000 in monolayer cultures of fetal rat neurons and in explant cultures of rat forebrain. The L1 polypeptide was co-translationally inserted into the membranes of the endoplasmic reticulum as an integral membrane protein. Both sulfation and phosphorylation of L1 was observed. L1 polypeptides with lower relative molecular weight which were present on the plasma membrane were probably derived from the 200,000 mol. wt polypeptide. The function of L1 was investigated and an L1 involvement in neurite fasciculation was demonstrated.

Comportement asymptotique des solutions d'équations elliptiques semi-linéaires dans RN

We study the asymptotic behaviour in RN of the solutions of the semilinear elliptic equation − Δu + u¦u¦q-1=f where q > 1 and f is a function of L1(RN) with compact support. We obtain three rates of decay according to the value of q by respect to N/(N - 2) and we prove that the behaviour of u is isotropic when q⩾(N+1)/(N− 1). We also give an asymptotic expansion of u in each case.

A best constant for Zygmund’s conjugate function inequality

When the space L log + L L{\log ^ + }L is given the Hardy-Littlewood norm the best constant in the corresponding version of Zygmund’s conjugate function inequality is shown to be \[ K = 1 − 2 − 3 − 2 + 5 − 2 − 7 − 2 + ⋯ 1 − 2 + 3 − 2 + 5 − 2 + 7 − 2 + ⋯ . {\mathbf {K}} = \frac {{{1^{ - 2}} - {3^{ - 2}} + {5^{ - 2}} - {7^{ - 2}} + \cdots }}{{{1^{ - 2}} + {3^{ - 2}} + {5^{ - 2}} + {7^{ - 2}} + \cdots }}. \] This complements the recent result of Burgess Davis that the best constant in Kolmogorov’s inequality is K − 1 {{\mathbf {K}}^{ - 1}} .

Integral equations associated with Hankel convolutions

1. Objectives. We denote by V[al, .., a,,] the number of variations of sign of the sequence a,, * , a,, of real numbers. Hence, for example, V[-1,0,I]=1, V[1,0,1]= 0, V[O,0,0]= -1. If f is a real function defined for 0 < x < cx, then V[f(x)] = l.u.b. V[f(xl), * ,f(x,,)], taken over all sets 0 X < X2< .< Let H be a real-valued function of L1(co, co), q a real-valued, continuous function of L0(c, co) and let