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Characterization of three distinct cDNA clones encoding cysteine proteinases from maize (Zea mays L.) callus.

In previous work, a 33 kDa cysteine proteinase was found in callus initiated from maize (Zea mays L.) resistant to fall armyworm feeding. A callus cDNA library from the maize inbred Mp708 was screened with oligonucleotides derived from the N-terminal amino acid sequence of the 33 kDa proteinase and several cDNA clones were isolated and sequenced. A cDNA clone encoding the 33 kDa cysteine proteinase, mir1, was identified. Two additional clones, mir2 and mir3, encoding putative cysteine proteinases were also identified. mir2 and mir3 are distinct from mir1 and each other, but show a high degree of homology. All of the mir cDNA clones map to distinct sites on the maize genome. Amino acid sequences encoded by the mir clones are similar to other known cysteine proteinases and are most closely related to the oryzain-alpha and -beta precursors. The ERFNIN motif and a 12 amino acid conserved sequence are present in the propeptide region of the putative proteinases encoded by mir clones. mir2 and mir3 appear to have C-terminal extensions. The phylogenetic tree of nucleotide sequences of mir1, mir2, mir3 and other representative cysteine proteinases from protozoa, plants and animals was constructed.

Amino Acid Sequence↗

The gene encoding the immunoregulatory signaling molecule CMRF-35A localized to human chromosome 17 in close proximity to other members of the CMRF-35 family.

The immunoregulatory signaling (IRS) family includes several molecules, which play major roles in the regulation of the immune response. The CMRF-35A and CMRF-35H molecules are two new members of the IRS family of molecules, that are found on a wide variety of haemopoietic lineages. The extracellular functional interactions of these molecules is presently unknown, although CMRF-35H can initiate an inhibitory signal and is internalized when cross-linked. In this paper, we described the gene structure for the CMRF-35A gene and its localization to human chromosome 17. The gene consists of four exons spanning approximately 4.5 kb. Exon 1 encodes the 5' untranslated region and leader sequence, exon 2 encodes the immunoglobulin (Ig)-like domain, exon 3 encodes the membrane proximal region and exon 4 encodes the transmembrane region, the cytoplasmic tail and the 3' untranslated region. A region in the 5' flanking sequence of the CMRF-35A gene, that promoted expression of a reporter gene was identified. The genes for the CMRF-35A and CMRF-35H molecules are closely linked on chromosome 17. Similarity between the Ig-like exons and the preceding intron of the two genes suggests exon duplication was involved in their evolution. We also identified a further member of the CMRF-35 family, the CMRF-35J pseudogene. This gene appears to have arisen by gene duplication of the CMRF-35A gene. These three loci - the CMRF-35A, CMRF-35J and CMRF-35H genes-form a new complex of IRS genes on chromosome 17.

3' Untranslated Regions↗

Feasibility of using genetic linkage analysis to identify the genes encoding T cell-defined minor histocompatibility antigens.

We have evaluated the utility of genetic linkage analysis to identify genes that encode minor histocompatibility antigens using vaccinia virus vectors as a simple and convenient method for transient expression of class I MHC molecules in lymphoblastoid cell lines. As a test case, we used a CTL clone that recognizes HA-8, a minor histocompatibility antigen encoded by the KIAA0020 gene and presented by HLA-A*0201. EBV-transformed B cell lines from individuals in three large pedigrees from the CEPH reference family collection were infected with a recombinant vaccinia virus vector encoding an HLA-A*0201 transgene, which led to high level expression of the MHC restricting allele HLA-A*0201 on the cell surface. HA-8 expression in the vaccinia-infected target cells was then determined using standard in vitro cytotoxicity assays. Pairwise linkage analysis of the segregation of HA-8 expression in these pedigrees demonstrated that the HA-8 gene was tightly linked with a cluster of marker loci located on the distal portion of chromosome 9p. Analysis of 9p marker haplotypes for individuals in the three families identified several individuals with recombinant haplotypes, and these recombination events were used to refine the precision of the HA-8 gene localization further. The data collectively indicate that the HA-8 gene is localized to a 10.3 cM (corresponding to 3.9 Mb) interval of distal 9p that is thought to encode at least 11 genes, including KIAA0020. These results demonstrate that linkage analysis can be used to map minor histocompatibility genes with high precision and accuracy. Over the next years, refinement and annotation of the human genome sequence will undoubtedly increase the utility of linkage analysis as a tool for identifying minor histocompatibility antigen genes.

Antigens, Surface↗

Self-perpetuating development of encoding biases in person perception.

It was hypothesized that encoding (interpretive) biases may develop in a self-perpetuating manner through biased, self-supportive encoding (even in the absence of any objectively supportive evidence). This process was investigated in 3 experiments with different stimulus materials (matrices of digits, silhouettes of persons, descriptions of personal problems). In the learning phase of each study, Ss nonconsciously acquired some encoding bias. In the testing phase, Ss' encoding of new material was predictably biased, and, consistent with the self-perpetuation hypothesis, the strength of the bias gradually increased over the segments of the material, even though the material did not contain any evidence supportive of the bias. Given the ambiguity of many (particularly social) stimuli, the self-perpetuation process may play a ubiquitous role in the development of interpretive categories and other individually differentiated cognitive dispositions.

Affect↗

Limitations of object-based feature encoding in visual short-term memory.

The present study investigated object-based feature encoding in visual short-term memory for 2 features within the same dimension that occur on different parts of an object. Using the change-detection paradigm, this experiment studied objects with 2 colors and objects with 2 orientations. Participants found it easier to monitor 1 rather than both features of such objects, even when decision noise was properly controlled for. However, no object-based benefit was observed for encoding the 2 features of each object that were of the same dimension. When similar stimuli were used but the 2 features of each object were from different dimensions (color and orientation), an object-based benefit was observed. These results thus impose a major constraint on object-based feature encoding theories by showing that only features from different dimensions can benefit from object-based encoding.

Adolescent↗

Divided attention and memory: evidence of substantial interference effects at retrieval and encoding.

In 5 divided attention (DA) experiments, students (24 in each experiment) performed visual distracting tasks (e.g., recognition of words, word and digit monitoring) while either simultaneously encoding an auditory word list or engaging in oral free recall of the target word list. DA during retrieval, using either of the word-based distracting tasks, produced relatively larger interference effects than the digit-monitoring task. DA during encoding produced uniformly large interference effects, regardless of the type of distracting task. Results suggest that when attention is divided at retrieval, interference is created only when the memory and concurrent task compete for access to word-specific representational systems; no such specificity is necessary to create interference at encoding. During encoding, memory and concurrent tasks compete primarily for general resources, whereas during retrieval, they compete primarily for representational systems.

Adult↗

Effects of age and a divided attention task presented during encoding and retrieval on memory.

The present studies were designed to examine age differences in memory when attention was divided during encoding, retrieval, or at both times. In Experiment 1, Ss studied categorized words while performing a number-monitoring task during encoding, retrieval, or at both times. Older Ss' free recall and clustering performance declined more than that of young Ss when attention was divided at encoding, but there was no similar age interaction when divided attention occurred at retrieval. In Experiment 2, the task demands at retrieval were increased by using a fast-paced, cued-recall task. The results remained unchanged from Experiment 1. Again, an age interaction occurred with divided attention at encoding but not at retrieval. These results were unexpected, given the emphasis in the memory-aging literature on increased difficulty of retrieval by older adults. The findings pose difficulties for limited processing resource views of age differences in memory.

Adult↗

Divided attention during encoding and retrieval: differential control effects?

Previous studies have shown that divided attention (DA) during retrieval has little effect on recall of episodic memories, although DA during encoding has a large detrimental effect. One possible reason for this asymmetry is that stimulus presentation at encoding is under experimenter control, whereas retrieval operations and responses are under participant control. This experiment tested this possibility by presenting paired-associate word lists for learning and recall, either at a fixed 4-s rate or at a rate controlled by the participant. The results showed that the higher recall levels for DA at retrieval than for DA at encoding held under all combinations of experimenter and participant control. The implications of these results for a fuller understanding of encoding and retrieval processes are discussed.

Adolescent↗

The effects of encoding task on age-related differences in the functional neuroanatomy of face memory.

Age-related differences in brain activity mediating face recognition were examined using positron emission tomography. Participants encoded faces using a pleasant-unpleasant judgment, a right-left orientation task, and intentional learning. Scans also were obtained during recognition. Both young and old groups showed signficant effects of encoding task on recognition accuracy, but older adults showed reduced accuracy overall. Increased brain activity in older adults was similar to that seen in young adults during conditions associated with deeper processing, but was reduced during the shallow encoding and recognition conditions. Left prefrontal activity was less in older adults during encoding, but greater during recognition. Differential correlations of brain activity and behavior were found that suggest older adults use unique neural systems to facilitate face memory.

Adult↗

Biased language use in stereotype maintenance: the role of encoding and goals.

In 4 studies, the authors investigated the relative impact of biased encoding of information and communication goals on biased language use. A category label (linguistic expectancy bias, Study 1) or a group label (linguistic intergroup bias, Study 2) was presented either before or after a story that participants were asked to communicate. Biased language use only emerged when participants learned about the group membership of the actor or the category label before hearing the story. However, communication goals had an effect on language use at the retrieval stage, independent of encoding (Studies 3 and 4). Although communication goal effects seemed to overwhelm encoding effects, encoding still influenced language use under externally imposed time pressure (Study 3) and self-imposed time constraints (Study 4). This research reaffirms the importance of both cognitive and communicative processes in stereotype maintenance and highlights the conditions under which they each operate.

Adult↗

Encoding and retrieval during bimanual rhythmic coordination.

In 2 experiments, bimanual 1:1 rhythmic coordination was performed concurrently with encoding or retrieval of word lists. Effects of divided attention (DA) on coordination were indexed by changes in mean relative phase and recurrence measures of shared activity between the 2 limbs. Effects of DA on memory were indexed by deficits in recall relative to baseline. For DA at both encoding and retrieval, the equilibrium values of relative phase were shifted and the degree of shared activity between left and right rhythmic motions was reduced. Recall was reduced, however, only for DA at encoding. The results corroborate and extend those obtained with more conventional secondary tasks (e.g., visual reaction time), suggesting attention dissimilarities between episodic encoding and retrieval.

Attention↗

A bacteriophage encoding a pathogenicity island, a type-IV pilus and a phage receptor in cholera bacteria.

The virulence properties of many pathogenic bacteria are due to proteins encoded by large gene clusters called pathogenicity islands, which are found in a variety of human pathogens including Escherichia coli, Salmonella, Shigella, Yersinia, Helicobacter pylori, Vibrio cholerae, and animal and plant pathogens such as Dichelobacter nodosus and Pseudomonas syringae. Although the presence of pathogenicity islands is a prerequisite for many bacterial diseases, little is known about their origins or mechanism of transfer into the bacterium. The bacterial agent of epidemic cholera, Vibrio cholerae, contains a bacteriophage known as cholera-toxin phage (CTXphi), which encodes the cholera toxin, and a large pathogenicity island called the VPI (for V. cholerae pathogenicity island) which itself encodes a toxin-coregulated pilus that functions as a colonization factor and as a CTXphi receptor. We have now identified the VPI pathogenicity island as the genome of another filamentous bacteriophage, VPIphi. We show that VPIphi is transferred between V. cholerae strains and provide evidence that the TcpA subunit of the toxin-coregulated type IV pilus is in fact a coat protein of VPIphi. Our results are the first description of a phage that encodes a receptor for another phage and of a virus-virus interaction that is necessary for bacterial pathogenicity.

Bacterial Outer Membrane Proteins↗

Genomic organization of the genes encoding mouse T-cell receptor alpha-chain.

The vertebrate immune system uses two kinds of antigen-specific receptors, the immunoglobulin molecules of B cells and the antigen receptors of T cells. T-cell receptors are formed by a combination of two different polypeptide chains, alpha and beta (refs 1-3). Three related gene families are expressed in T cells, those encoding the T-cell receptor, alpha and beta, and a third, gamma (refs 4-6), whose function is unknown. Each of these polypeptide chains can be divided into variable (V) and constant (C) regions. The V beta regions are encoded by V beta, diversity (D beta) and joining (J beta) gene segments that rearrange in the differentiating T cell to generate V beta genes. The V gamma regions are encoded by V gamma, J gamma and, possibly, D gamma gene segments. Studies of alpha complementary DNA clones suggest that alpha-polypeptides have V alpha and C alpha regions and are encoded by V alpha and J alpha gene segments and a C alpha gene. Elsewhere in this issue we demonstrate that 18 of 19 J alpha sequences examined are distinct, indicating that the J alpha gene segment repertoire is much larger than those of the immunoglobulin (4-5) or beta (14) gene families. Here we report the germline structures of one V alpha and six J alpha mouse gene segments and demonstrate that the structures of the V alpha and J alpha gene segments and the alpha-recognition sequences for DNA rearrangement are similar to those of their immunoglobulin and beta-chain counterparts. We also show that the J alpha gene-segment organization is strikingly different from that of the other immunoglobulin and rearranging T-cell gene families. Eighteen J alpha gene segments map over 60 kilobases (kb) of DNA 5' to the C alpha gene.

Amino Acid Sequence↗

A Drosophila Minute gene encodes a ribosomal protein.

Minute genes have long constituted a special problem in Drosophila genetics. For at least 50-60 different genes scattered throughout the genome, dominant mutations and/or deficiencies have been recognized which result in a common phenotype consisting of short thin bristles, slow development, reduced viability, rough eyes, small body size and etched tergites. Schultz proposed that the Minute loci encode similar but separate functions involved in growth and division common to all cells. Atwood and Ritossa suggested that Minute loci encode components of the protein synthetic machinery, specifically the transfer RNA genes; this now seems unlikely on grounds of both mapping and mutability studies. More recently, we and others suggested that the Minute loci are ribosomal protein genes. We report here that transformation with a cloned 3.3-kilobase (kb) region containing the gene encoding the large subunit ribosomal protein 49 (rp49) suppresses the dominant phenotypes of Minute (3)99D, a previously undescribed Minute associated with a chromosomal deficiency of the 99D interval. This activity is specific to the 99D Minute as it does not suppress other Minute loci elsewhere in the genome. This result provides direct evidence that the Minute locus at the 99D interval encodes the ribosomal protein 49.

Animals↗

A maternally inherited superantigen encoded by a mammary tumour virus.

A collection of superantigens, molecules which in combination with class II major histocompatibility complex (MHC) engage T cells bearing particular V beta chains as part of their alpha beta receptors, have recently been described. The mouse self superantigen, Mls-1a, for example, in conjunction with many MHC class II proteins, engages mouse T cells bearing V beta 6, 7, 8.1 and 9, almost regardless of the sequences of the other variable components of the receptors on the T cells. Two types of superantigen have been identified so far: first, superantigens encoded in the mouse genome, such as Mls-1a; second, superantigens produced by bacteria, such as the staphylococcal enterotoxins. Although the latter type of superantigens are in many cases known to be proteins of about 220 amino acids, nothing is known about the structures of any of the superantigens encoded in mouse. Here we describe the properties of a new mouse superantigen. The antigen is maternally transmitted in milk and is probably encoded by a mammary tumour virus (MTV). Given the known genetic linkage between at least one of the mouse genomic superantigens and endogenous MTV integration sites, it is tempting to speculate that the superantigen described here and some of the endogenous mouse superantigens are encoded by MTVs.

Animals↗

Genes encoding ligands for deletion of V beta 11 T cells cosegregate with mammary tumour virus genomes.

The T-cell receptor (TCR) repertoire is selected in the thymus after rearrangement of genes encoding TCR alpha and beta chains. Selection is based on the recognition by newly emergent T cells of self-ligands associated with molecules of the major histocompatibility complex: some combinations result in positive selection, others in negative selection. Negative selection, or clonal deletion, is an important mechanism for eliminating autoreactive T cells. A group of self-ligands involved in clonal deletion was identified because they, like exogenous superantigens, were recognized by almost all T cells expressing particular TCR V beta genes. V beta 17a T cells are deleted by a tissue-specific ligand; V beta 6, V beta 7, V beta 8.1 and V beta 9 T cells are deleted by the minor lymphocyte-stimulating (Mls) determinant Mls-1a; V beta 3 T cells by Mls-2a and Mls-3a; V beta 11 T cells by ligands encoded by independently segregating genes; and V beta 5 T cells by ligands encoded by two genes. Chromosome mapping using recombinant inbred strains of mice and classic backcrosses show that Mls-1a in DBA/2 mice is encoded on chromosome 1, that one of the two ligand genes for deletion of V beta 5 T cells maps to chromosome 12 and that a ligand gene for V beta 11 deletion is linked to the CD8 locus on chromosome 6. Here we present evidence from three sets of backcross mice for concordance between V beta 11 deletion ligand genes on chromosomes 6, 12 and 14 and endogenous mouse mammary tumour virus integrant (Mtv) genomes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The Pendred syndrome gene encodes a chloride-iodide transport protein.

Pendred syndrome is the most common form of syndromic deafness and characterized by congenital sensorineural hearing loss and goitre. This disorder was mapped to chromosome 7 and the gene causing Pendred syndrome (PDS) was subsequently identified by positional cloning. PDS encodes a putative transmembrane protein designated pendrin. Pendrin is closely related to a family of sulfate transport proteins that includes the rat sulfate-anion transporter (encoded by Sat-1; 29% amino acid sequence identity), the human diastrophic dysplasia sulfate transporter (encoded by DTD; 32%) and the human sulfate transporter 'downregulated in adenoma' (encoded by DRA; 45%). On the basis of this homology and the presence of a slightly modified sulfate-transporter signature sequence comprising its putative second transmembrane domain, pendrin has been proposed to function as a sulfate transporter. We were unable to detect evidence of sulfate transport following the expression of pendrin in Xenopus laevis oocytes by microinjection of PDS cRNA or in Sf9 cells following infection with PDS-recombinant baculovirus. The rates of transport for iodide and chloride were significantly increased following the expression of pendrin in both cell systems. Our results demonstrate that pendrin functions as a transporter of chloride and iodide, but not sulfate, and may provide insight into thyroid physiology and the pathophysiology of Pendred syndrome.

Animals↗

Glutamate-receptor-mediated encoding and retrieval of paired-associate learning.

Paired-associate learning is often used to examine episodic memory in humans. Animal models include the recall of food-cache locations by scrub jays and sequential memory. Here we report a model in which rats encode, during successive sample trials, two paired associates (flavours of food and their spatial locations) and display better-than-chance recall of one item when cued by the other. In a first study, pairings of a particular foodstuff and its location were never repeated, so ensuring unique 'what-where' attributes. Blocking N-methyl-d-aspartate receptors in the hippocampus--crucial for the induction of certain forms of activity-dependent synaptic plasticity--impaired memory encoding but had no effect on recall. Inactivating hippocampal neural activity by blocking alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors impaired both encoding and recall. In a second study, two paired associates were trained repeatedly over 8 weeks in new pairs, but blocking of hippocampal AMPA receptors did not affect their recall. Thus we conclude that unique what-where paired associates depend on encoding and retrieval within a hippocampal memory space, with consolidation of the memory traces representing repeated paired associates in circuits elsewhere.

2-Amino-5-phosphonovalerate↗