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PubMedDate not supplied

Aging, encoding, and word retrieval: distinguishing phonological and memory processes.

Word retrieval deficits are one of the most common complaints among older adults. The Transmission Deficit Hypothesis predicts that phonologically similar names would be harder for older adults to encode and retrieve. Results indicated that overall older adults encoded and recalled fewer words than younger adults when given only one trial and when given multiple trials to criterion. For both experiments, proper names were more difficult to retrieve than common nouns, and phonologically similar words were more difficult to retrieve than phonologically different words for both older and younger adults. Age differences were not evident for retrieving phonologically similar items or names but older adults did need more trials to encode phonologically similar items and names. Age differences for phonologically similar items and names appear related to encoding processes with retrieval of these items consistently hard for both older and younger adults.

Adolescent↗

PubMed1983

Age differences in cued recall and recognition under varying encoding and retrieval conditions.

This experiment investigated the role of the encoding-retrieval relationship in adult age differences in memory. To determine the optimal encoding-retrieval conditions for adults of different ages, young, middle-aged, and older adults were given a semantic or acoustic orienting task, followed by semantic and acoustic recognition tests or semantic and acoustic cued recall tests. As predicted, the results demonstrated the importance of similar encoding and retrieval conditions at all ages, especially with semantic processing. Age differences were reduced on the recognition test and when semantic encoding was combined with a semantic cue test at retrieval. It was concluded that acoustic processing is not as effective as semantic processing for older or younger adults, and that effective use of semantic processing by older adults depends on constrained task conditions. These conditions include congruent semantic orienting questions that specify precise meanings for each target item, and retrieval cues that match the information in the orienting questions.

Adult↗

PubMedDate not supplied

Effects of phonemic awareness instruction on the encoding skills of children with severe speech impairment.

PURPOSE: To examine the effects of phoneme-grapheme correspondence and phonemic awareness instruction on the encoding abilities of three pre-reading children with severe speech impairment (SSI). METHOD: Using a single subject multiple baseline design across behaviours and participants, children received phoneme-grapheme awareness instruction followed by instruction in segmenting, manipulating, and encoding consonant-vowel-consonant (CVC) pseudowords. RESULTS: Generalization occurred to encoding of novel CVC pseudo- and real words for two of the three participants. CONCLUSIONS: Results suggest that phoneme-grapheme correspondence and phonemic awareness instruction is effective in developing encoding skills in children with SSI. Findings are consistent with those for other at-risk children.

Articulation Disorders↗

PubMed1995

Age differences in reported recollective experience are due to encoding effects, not response bias.

Three experiments examined whether reduced recollective experience reported in old age is due to a criterion shift towards more cautious responses by older subjects. In Experiment 1 Young and Old subjects took a recognition test without specific instructions on how they should encode the presented words. For recognised items subjects indicated whether they recollected the item's previous occurrence or whether they just knew it had been on the list. They then rated their confidence that the word came from the study list. Although overall recognition levels were equivalent, older adults recollected less and reported more know responses than the younger subjects. However, there was no overall difference in confidence, contrary to a criterion shift explanation. In Experiment 2A specific encoding instructions removed the age-related change in recollective experience entirely. Experiment 2B reproduced the test conditions of Experiment 2A, but without specific encoding instructions, and replicated the pattern of know responding found in Experiment 1. Thus the three experiments together suggest that the amount of recollection experienced by the elderly is not explicable in terms of cautiousness, but is driven by the encoding carried out by the elderly at presentation.

Age Factors↗

PubMed2004

Comprehension, encoding, and monitoring in the production of confabulation in memory: a study with schizophrenic patients.

INTRODUCTION: The aim of the present study was to test the hypotheses proposed by Nathaniel-James and collaborators (Nathaniel-James & Frith, 1996; Nathaniel-James, Foong, & Frith, 1996) to account for the cognitive deficits involved in the production of confabulations in schizophrenic patients: impairments in comprehension, memory encoding, and memory monitoring. METHOD: Five patients were investigated in this multiple single-case study. Comprehension abilities were investigated in several tests in which a memory bias was avoided. The encoding deficit hypothesis was tested by manipulating cues at encoding and/or retrieval. "Memory monitoring" abilities were examined in two tasks: the Hayling test for all patients and an AB-AC word pairs learning task for two patients. RESULTS: Four of the patients produced an abnormal level of confabulations in story and fable learning tests. All patients exhibited encoding deficits and specific comprehension difficulties. However, some demonstrated preserved memory monitoring abilities. Across different tests, it was observed that the more the confabulations occurred, the more severe were the comprehension difficulties. CONCLUSION: The results are in favour of the hypothesis that verbal comprehension difficulties lead to the production of confabulation. They are inconsistent with the idea that memory monitoring impairment is necessarily involved.

Journal Article↗

PubMedDate not supplied

Episodic encoding in normal aging: attentional resources hypothesis extended to musical material.

The goal of the present study was to examine age-related changes in musical episodic memory for novel tunes. This was conducted by manipulating the encoding condition in a recognition paradigm. After receiving memory instructions (intentional condition), older and younger participants obtained equivalent hits. In contrast, when intentional encoding was accompanied by a dancing judgment (dancing + intentional condition), the recognition performance of the older persons was severely impaired. Impaired recognition was also found when participants only judged the excerpts without being instructed to memorize them (dancing judgment condition). Although older participants demonstrated a preserved ability to perform the dancing judgment on its own, this ability was not optimal and likely precluded the initiation of more elaborate encoding strategies. These results suggest that asking older persons to divide their attention in the study phase reduces the quality of their musical encoding. Given this extension to musical material, we discuss the notion that the age-related attentional resource decline appears to be domain-general rather than specific to verbal material.

Adult↗

PubMed1986

A cloned cDNA encoding MAP1 detects a single copy gene in mouse and a brain-abundant RNA whose level decreases during development.

Screening of a bacteriophage lambda gt11 cDNA expression library with a polyclonal anti-microtubule associated protein (MAP) antiserum resulted in the isolation of two non-cross-hybridizing sets of cDNA clones. One set was shown to encode MAP2 (Lewis, S. A., A. Villasante, P. Sherline, and N. J. Cowan, 1986, J. Cell Biol., 102:2098-2105). To determine the specificity of the second set, three non-overlapping fragments cloned from the same mRNA molecule via a series of "walking" experiments were separately subcloned into inducible plasmid expression vectors in the appropriate orientation and reading frame. Upon induction and analysis by immunoblotting, two of the fusion proteins synthesized were shown to be immunoreactive with an anti-MAP1-specific antibody, but not with an anti-MAP2-specific antibody. Since these MAP1-specific epitopes are encoded in non-overlapping cDNAs cloned from a single contiguous mRNA, these clones cannot encode polypeptides that contain adventitiously cross-reactive epitopes. Furthermore, these cDNA clones detected an abundant mRNA species of greater than 10 kb in mouse brain, consistent with the coding requirement of a 350,000-D polypeptide and the known abundance of MAP1 in that tissue. The MAP1-specific cDNA probes were used in blot transfer experiments with RNA prepared from brain, liver, kidney, stomach, spleen, and thymus. While detectable quantities of MAP1-specific mRNA were observed in these tissues, the level of MAP1 expression was approximately 500-fold lower than in brain. The levels of both MAP1-specific and MAP2-specific mRNAs decline in the postnatal developing brain; the level of MAP1-specific mRNA also increases slightly in rat PC12 cells upon exposure to nerve growth factor. These surprising results contrast sharply with reported dramatic developmental increases in the amount of MAP1 in brain and in nerve growth factor-induced PC12 cells. The cDNA clones encoding MAP1 detect a single copy sequence in mouse DNA, even under conditions of low stringency that would allow the detection of related but mismatched sequences. The cDNAs cross-hybridize with genomic sequences in rat, human, and chicken DNA, but not with DNA from frog, Drosophila, or sea urchin. These data are discussed in terms of the evolution and possible biological role of MAP1.

Animals↗

PubMed1991

Isolation and characterization of cDNAs encoding human brain ankyrins reveal a family of alternatively spliced genes.

Ankyrins are a family of membrane-associated proteins that can be divided into two immunologically distinct groups: (a) erythrocyte-related isoforms (ankyrinR) that have polarized distributions in particular cell types; and (b) brain-related isoforms (ankyrinB) that display a broader distribution. In this paper, we report the isolation and sequences of cDNAs related to two ankyrinB isoforms, human brain ankyrin 1 and 2, and show that these isoforms are produced from alternatively spliced mRNAs of a single gene. Human brain ankyrin 1 and 2 share a common NH2-terminus that is similar to human erythrocyte ankyrins, with the most striking conservation occurring between areas composed of a repeated 33-amino acid motif and between areas corresponding to the central portion of the spectrin-binding domain. In contrast, COOH-terminal sequences of brain ankyrin 1 and 2 are distinct from one another and from human erythrocyte ankyrins, and thus are candidates to mediate protein interactions that distinguish these isoforms. The brain ankyrin 2 cDNA sequence includes a stop codon and encodes a polypeptide with a predicted molecular mass of 202 kD, which is similar to the Mr of the major form of ankyrin in adult bovine brain membranes. Moreover, an antibody raised against the conserved NH2-terminal domain of brain ankyrin cross-reacts with a single Mr = 220 kD polypeptide in adult human brain. These results strongly suggest that the amino acid sequence of brain ankyrin 2 determined in this report represents the complete coding sequence of the major form of ankyrin in adult human brain. In contrast, the brain ankyrin 1 cDNAs encode only part of a larger isoform. An immunoreactive polypeptide of Mr = 440 kD, which is evident in brain tissue of young rats, is a candidate to be encoded by brain ankyrin 1 mRNA. The COOH-terminal portion of brain ankyrin 1 includes 15 contiguous copies of a novel 12-amino acid repeat. Analysis of DNA from a panel of human/rodent cell hybrids linked this human brain ankyrin gene to chromosome 4. This result, coupled with previous reports assigning the human erythrocyte ankyrin gene to chromosome 8, demonstrates that human brain and erythrocyte ankyrins are encoded by distinct members of a multigene family.

Amino Acid Sequence↗

PubMed1984

Sequence of a cDNA encoding Basilea kappa light chains (K2 isotype) suggests a possible relationship of protein structure to limited expression.

We present the complete sequence of a cDNA encoding rabbit immunoglobulin kappa light chains of the Basilea isotype (K2). Although all rabbits seem to possess a K2 constant region gene, expression of this gene in most rabbits is minimal if present at all. Even in Basilea rabbits the majority of expressed immunoglobulins are of lambda type. We find that the sequence of our Basilea cDNA constant region and the sequence of a "silent" K2 gene from b4 rabbits (bas-N4) are almost identical. The bas (K2) isotype lacks cysteine at position 171 in the constant region that is present in all K1 constant regions and usually forms an interdomain disulfide bond, with a cysteine at position 80 of the variable region. We postulate that one factor contributing to the low expression of the bas (K2) isotype could be a paucity of V kappa regions lacking cysteine at position 80. If a typical rabbit V kappa encoding Cys at position 80 is rearranged and expressed with th K2 isotype. B cells with mRNAs encoding light chains with free sulfhydryl groups would result. These cells may fail to form functional immunoglobulin receptors. Only a small subset of rabbit variable regions that lack the cysteine at position 80 would rearrange and encode K2 light chains lacking a free sulfhydryl group.

Amino Acid Sequence↗

PubMed1988

A high proportion of T lymphocytes that infiltrate H-2-incompatible heart allografts in vivo express genes encoding cytotoxic cell-specific serine proteases, but do not express the MEL-14-defined lymph node homing receptor.

The role of cytotoxic cells in in vivo immune functions such as allograft rejection is unknown. To begin to assess the function of cytolytic cells in vivo we have begun with cytolytic cell-specific functional molecules: we have isolated and characterized cytolytic cell-specific cDNA clones from cytolytic T cell clones, both encoding distinct serine esterases. The HF gene encodes a trypsin-like enzyme while the C11 gene encodes an enzyme with likely specificity for acidic residues. Here we demonstrate, using in situ hybridization with RNA probe, that both genes are expressed selectively in a subset of T lymphocytes that have infiltrated cardiac allografts. The phenotype of these cells is consistent with the most frequent phenotype of active CTL raised in vitro: they are predominantly CD4-, CD8+, MEL-14- T cell blasts. Thus the expression of these genes, each of which encodes serine esterase found in killer cell granules in vitro, is a valid marker for these cells in vivo as well. The kinetics of their accumulation is consistent with, but not proof of, a putative role in allograft rejection. It is likely that HF and C11 gene expression will be of diagnostic value.

Animals↗

PubMed1993

Human T cells respond to mouse mammary tumor virus-encoded superantigen: V beta restriction and conserved evolutionary features.

Mouse mammary tumor virus (MMTV)-encoded superantigens (SAGs) influence the murine T cell repertoire and stimulate a strong mixed lymphocyte response in vitro. These SAGs are encoded by the open reading frame of the 3' long terminal repeat of MMTV, termed MMTV SAGs. The T cell response to MMTV SAGs is V beta restricted and requires expression of the class II molecules of the major histocompatibility complex (MHC) on the presenting cells. While human T cells respond to bacterial SAGs, it is not known if human T cells or human MHC class II molecules can interact with MMTV SAGs. A fibroblastic cell line expressing the human MHC class II molecule HLA-DR1 and the Mtv-7 sag gene encoding Mls-1 was used to stimulate human T cells. We show here that human T cells efficiently proliferate in response to Mls-1 presented by HLA-DR1. This T cell response was inhibited by mAbs directed against CD4 or MHC class II molecules but not by mAbs specific for CD8 or MHC class I molecules. Moreover, the response to Mls-1 was limited to human T cells expressing a restricted set of T cell receptor V beta chains. Human T cells expressing V beta 12, 13, 14, 15, and 23 were selectively amplified after Mtv-7 sag stimulation. Interestingly, these human V beta s share the highest degree of homology with the mouse V beta s interacting with Mls-1. These results show a strong evolutionary conservation of the structures required for the presentation and the response to retrovirally encoded endogenous SAGs, raising the possibility that similar elements operate in humans to shape the T cell repertoire.

Animals↗

PubMed1995

The class I-b molecule Qa-1 forms heterodimers with H-2Ld and a novel 50-kD glycoprotein encoded centromeric to I-E beta.

Recent biochemical characterization of the T23-encoded Qa-1 molecule revealed an additional higher molecular mass species of 50 kD coprecipitated with the 48-kD Qa-1 molecule in H-2b and H-2d mouse strains. We now demonstrate that the 50-kD protein coprecipitated with Qa-1 is the class I-a antigen Ld in all H-2Ld-positive mouse strains examined. Furthers analyses of a panel of recombinants revealed that the 50-kD protein coprecipitated with Qa-1 in H-2b haplotype mouse strains is encoded or controlled by a gene centromeric to major histocompatibility complex class II I-E beta. We have designated this gene and corresponding protein product as Qsm, Qa-1 structure modifier. Both Ld and Qsm can interact with Qa-1 to form cell surface-expressed heterodimers in vivo. These Qa-1 heterodimers are not expressed in H-2k haplotype cells. The Qa-1/Ld and Qa-1/Qsm heterodimers are associated by noncovalent interactions and occur only between fully processed proteins. In addition, we show that the Qsm-encoded protein can form heterodimers with Ld as well, and that the Ld molecules participating in these interactions with Qa-1 and Qsm may be devoid of beta 2-microglobulin and/or peptide. These data represent the first demonstration that class I molecules can be expressed as heterodimers (Qa-1/Ld) on the cell surface, and map a gene (Qsm) that may potentially encode a novel class I molecule, or another protein, that associates with both Qa-1 and Ld. These interactions may enable increased levels of Qa-1 to reach the cell surface and may subsequently influence T cell recognition of Qa-1 and/or Ld molecules.

Animals↗

PubMed1995

52-kD SS-A/Ro: genomic structure and identification of an alternatively spliced transcript encoding a novel leucine zipper-minus autoantigen expressed in fetal and adult heart.

The 52-kD SS-A/Ro protein is one of the antigenic targets strongly associated with the autoimmune response in mothers whose children have manifestations of neonatal lupus. In addition to the cDNA clone we previously reported for the full-length 52-kD SS-A/Ro protein, an interesting MOLT-4 cDNA clone, p52-2, was found to have an internal deletion of 231 nucleotides including the domain encoding the leucine zipper motif. To further investigate the nature of this deletion, genomic DNA clones were isolated from a lambda FIXII library. The complete gene for the full-length 52-kD protein (alpha form, 52 alpha) spans 10 kb of DNA and is composed of seven exons. Exon 1 contains only the 5' untranslated sequence, while the translation initiation codon is located 3 kb downstream in exon 2, which also encodes the three zinc finger motifs. Exon 4 encodes amino acids 168-245, including the coiled coil/leucine zipper domain. Exon 7 is the longest and encodes the rfp-like domain and the 3' untranslated region. The cDNA p52-2 can now be accounted for as a product of alternative messenger RNA (mRNA) derived from the splicing of exon 3 to exon 5, skipping exon 4, which results in a smaller protein (52 beta) with a predicted molecular weight of 45,000. An initial approach to identifying this alternatively spliced form in the human heart used a ribonuclease protection assay. Using an RNA probe corresponding to bases 674-964 of the full-length cDNA, two protected mRNA fragments were identified, a 290-bp fragment corresponding to expression of 52 alpha and a smaller fragment of 144 bp, the predicted size of 52 beta. Using reverse transcription followed by polymerase chain reaction, cDNAs from a 16-wk fetal heart, 24-wk heart, and adult heart were amplified with primers flanking exon 4. Two polymerase chain reaction products were observed in each tissue, one 1.0 kb likely representing 52 alpha and a second 0.78 kb, consistent with 52 beta. The 0.78-kb fragment identified in the 16-wk heart was cloned, and DNA sequencing confirmed the 52 beta type. Immunoprecipitation of in vitro-translated 35S-labeled 52 beta form was performed to evaluate the antigenicity of this novel form of 52-kD SS-A/Ro. 26 (87%) of 30 sera tested from mothers whose children were known to have neonatal lupus immunoprecipitated the 52 beta form.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed2003

Identification of a polymorphic gene, BCL2A1, encoding two novel hematopoietic lineage-specific minor histocompatibility antigens.

We report the identification of two novel minor histocompatibility antigens (mHAgs), encoded by two separate single nucleotide polymorphisms on a single gene, BCL2A1, and restricted by human histocompatibility leukocyte antigen (HLA)-A*2402 (the most common HLA-A allele in Japanese) and B*4403, respectively. Two cytotoxic T lymphocyte (CTL) clones specific for these mHAgs were first isolated from two distinct recipients after hematopoietic cell transplantation. Both clones lyse only normal and malignant cells within the hematopoietic lineage. To localize the gene encoding the mHAgs, two-point linkage analysis was performed on the CTL lytic patterns of restricting HLA-transfected B lymphoblastoid cell lines obtained from Centre d'Etude du Polymorphisme Humain. Both CTL clones showed a completely identical lytic pattern for 4 pedigrees and the gene was localized within a 3.6-cM interval of 15q24.3-25.1 region that encodes at least 46 genes. Of those, only BCL2A1 has been reported to be expressed in hematopoietic cells and possess three nonsynonymous nucleotide changes. Minigene transfection and epitope reconstitution assays with synthetic peptides identified both HLA-A*2402- and B*4403-restricted mHAg epitopes to be encoded by distinct polymorphisms within BCL2A1.

Amino Acid Sequence↗

PubMed1997

Autosomal recessive phosphorylase kinase deficiency in liver, caused by mutations in the gene encoding the beta subunit (PHKB).

The association of autosomal recessive phosphorylase kinase deficiency in liver of a 3 1/2-year-old female child with mutations in the gene encoding the common part of the beta subunit of phosphorylase kinase is reported. The proband had a severe deficiency of phosphorylase kinase in liver, while the phosphorylase kinase activity in erythrocytes was only slightly diminished. She had no symptoms of muscle involvement. The complete coding sequences of the liver gamma subunit and of the beta subunit of phosphorylase kinase of the proband were analyzed for the presence of mutations, by either reverse-transcribed PCR or SSCP analysis. Three deviations from the normal sequence were found in the region encoding the common part of the beta subunit of phosphorylase kinase-namely, a 1827G-->A (W609X) transition, a 2309A-->G (Y770C) transition, and a deletion of nucleotides 2896-2911-whereas no mutations were detected in the sequence encoding the liver gamma subunit of phosphorylase kinase. The 1827G-->A mutation and the deletion both result in the formation of early stop codons. Investigation of DNA showed that the deletion is caused by a splice-acceptor site mutation (IVS30(-1),g-->t). Family analysis revealed that the 1827G-->A and IVS30(-1),g-->t substitutions are located on different parental chromosomes and that compound heterozygosity for these mutations segregates with the disease. The 2309A-->G mutation was detected in 2%-3% of the normal population. Thus, it is concluded that the deficiency of phosphorylase kinase in this proband is caused by compound heterozygosity for the 1827G-->A and the IVS30(-1),g-->t mutations and that the 2309A-->G mutation is a polymorphism. This implies that a defect in the sequence encoding the common part of the beta subunit of phosphorylase kinase may present as liver phosphorylase kinase deficiency.

Carbohydrate Metabolism, Inborn Errors↗

PubMed2000

The MHC class I heavy chain is a common target of the small proteins encoded by the 3' end of HTLV type 1 and HTLV type 2.

Human T cell leukemia/lymphotropic virus types 1 and 2 are two immunologically and phylogenetically related retroviruses that differ in their pathogenicity in vivo. The overall genetic structure of HTLV-1 and -2 is similar. Each contains a unique region at the 3' end of the genome, designated the pX region. p12(I) is a membrane-associated protein encoded by the open reading frame I (ORF I) region of HTLV-1, which lies within the pX region. A corresponding protein, p10(I) is encoded by the ORF I region of HTLV-2 and an additional protein, p11(V), is encoded by ORF V, which overlaps the HTLV-2 ORF I region. As with HTLV-1, the small proteins encoded by the pX region of HTLV-2 appear to be dispensable for viral replication and cellular transformation in vitro. However, the small open reading frames of both viruses are important for viral replication in vivo, which suggests they may play an important role during the viral life cycle. This study was undertaken to investigate and compare the cellular targets of the p10(I), p11(V), and p12(I) putative proteins.

3' Untranslated Regions↗

PubMed2000

Structure and expression of the mouse gene encoding the orphan nuclear receptor TEC.

Translocated in extraskeletal chondrosarcoma (TEC) is an orphan nuclear receptor involved in the control of cell proliferation and apoptosis and is expressed mainly in the mammalian central nervous system. To help understand the regulation of its expression, we have characterized the mouse genomic locus encoding TEC and analyzed its expression pattern in various tissues. The gene spans approximately 40 kb and contains 8 exons, of which the first two are noncoding. The promoter region does not contain any identifiable TATA box or CCAAT box elements; however, several binding sites for the transcription factors cyclic AMP-responsive element binding (CREB) protein and Spl are present. Two types of transcripts generated by alternative splicing were characterized by RT-PCR: one encodes the full-length receptor of 627 amino acids; the other encodes a truncated receptor of 429 amino acids lacking the entire carboxyl-terminal domain. Northern blots and RT-PCR analyses showed that mRNAs encoding both isoforms are expressed in all mouse tissues examined, with the highest levels being found in the brain. This expression pattern suggests that TEC may perform some basic housekeeping cellular function in addition to its role in cell proliferation.

Amino Acid Sequence↗

PubMedDate not supplied

Homology between the cDNAs encoding phosphoprotein p19 and SCG10 reveals a novel mammalian gene family preferentially expressed in developing brain.

We have isolated and sequenced a rat testis cDNA encoding p19, a 19-kD cytosolic phosphoprotein that is abundant in immature brain, testis, and neuroendocrine tumor cells. The cDNA was identified using bovine brain p19 peptide sequences, which indicate that the gene encoding p19 has been highly conserved during mammalian evolution. Using Northern blot analysis on rat tissues, p19 mRNA was readily detected in brain and testis and showed a 15-fold greater abundance in newborn than in adult brain. Low levels of p19 mRNA were observed in spleen, kidney, and heart, but not in liver. Thus, the expression of the gene encoding p19 shows a strong tissue preference and is developmentally regulated. The predicted amino acid sequence of p19 is highly homologous to that of SCG10, another protein expressed in the developing rat nervous system, suggesting that the two proteins serve similar functions. Based on a comparison of the two cDNAs, we conclude that p19 and SCG10 are encoded by distinct but related genes constituting a novel gene family.

Aging↗