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Schematic memories develop quickly, but are not expressed unless necessary.

ABSTRACT: Episodic memory retrieval is increasingly influenced by schematic information as memories mature, but it is unclear whether this is due to the slow formation of schemas over time, or the slow forgetting of the episodes. To address this, we separately probed memory for newly learned schemas as well as their influence on episodic memory decisions. In this experiment, participants encoded images from two categories, with the location of images in each category drawn from a different spatial distribution. They could thus learn schemas of category locations by encoding specific episodes. We found that images that were more consistent with these distributions were more precisely retrieved, and this schematic influence increased over time. However, memory for the schema distribution, measured using generalization to novel images, also became less precise over time. This incongruity suggests that schemas form rapidly, but their influence on episodic retrieval is dictated by the need to bolster fading memory representations.

SUBMITTER: Tompary A

PROVIDER: S-EPMC7550328 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Schematic memories develop quickly, but are not expressed unless necessary.

Tompary Alexa A Zhou WenXi W Davachi Lila L

Scientific reports 20201012 1

Episodic memory retrieval is increasingly influenced by schematic information as memories mature, but it is unclear whether this is due to the slow formation of schemas over time, or the slow forgetting of the episodes. To address this, we separately probed memory for newly learned schemas as well as their influence on episodic memory decisions. In this experiment, participants encoded images from two categories, with the location of images in each category drawn from a different spatial distrib ...[more]

PMID: 33046766

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Project description:BackgroundThe giant sarcomere protein titin is important in both heart health and disease. Mutations in the gene encoding for titin (TTN) are the leading known cause of familial dilated cardiomyopathy. The uneven distribution of these mutations within TTN motivated us to seek a more complete understanding of this gene and the isoforms it encodes in cardiomyocyte (CM) sarcomere formation and function.MethodsTo investigate the function of titin in human CMs, we used CRISPR/Cas9 to generate homozygous truncations in the Z disk (TTN-Z-/-) and A-band (TTN-A-/-) regions of the TTN gene in human induced pluripotent stem cells. The resulting CMs were characterized with immunostaining, engineered heart tissue mechanical measurements, and single-cell force and calcium measurements.ResultsAfter differentiation, we were surprised to find that despite the more upstream mutation, TTN-Z-/--CMs had sarcomeres and visibly contracted, whereas TTN-A-/--CMs did not. We hypothesized that sarcomere formation was caused by the expression of a recently discovered isoform of titin, Cronos, which initiates downstream of the truncation in TTN-Z-/--CMs. Using a custom Cronos antibody, we demonstrate that this isoform is expressed and integrated into myofibrils in human CMs. TTN-Z-/--CMs exclusively express Cronos titin, but these cells produce lower contractile force and have perturbed myofibril bundling compared with controls expressing both full-length and Cronos titin. Cronos titin is highly expressed in human fetal cardiac tissue, and when knocked out in human induced pluripotent stem cell derived CMs, these cells exhibit reduced contractile force and myofibrillar disarray despite the presence of full-length titin.ConclusionsWe demonstrate that Cronos titin is expressed in developing human CMs and is able to support partial sarcomere formation in the absence of full-length titin. Furthermore, Cronos titin is necessary for proper sarcomere function in human induced pluripotent stem cell derived CMs. Additional investigation is necessary to understand the molecular mechanisms of this novel isoform and how it contributes to human cardiac disease.

Project description:Mustn1 encodes a small nuclear protein expressed specifically in the musculoskeletal system that was originally identified as a strongly up-regulated gene during bone regeneration, especially in fracture callus proliferating chondrocytes. Further experiments were undertaken to investigate its expression and role during chondrogenesis. Initially, whole mount mouse in situ hybridization was carried out and revealed Mustn1 expression in areas of active chondrogenesis that included limb buds, branchial arches and tail bud. To elucidate its function, experiments were carried out to perturb Mustn1 by overexpression and silencing in the pre-chondrocytic RCJ3.1C5.18 (RCJ) cell line. In these cells, Mustn1 is normally differentially regulated, with a spike in expression 2 days after induction of differentiation. Further, Mustn1 was successfully overexpressed in multiple RCJ cell lines by approximately 2-6 fold, and reduced to approximately 32-52% in silenced cell lines as compared to parental Mustn1 levels. Overexpressing, silenced, control, and parental RCJ cell lines were assayed for proliferation and differentiation. No statistically significant changes were observed in either proliferation or proteoglycan production when Mustn1 overexpressing lines were compared to parental and control. By contrast, both proliferation rate and differentiation were significantly reduced in Mustn1 silenced cell lines. Specifically, RNAi silenced cell lines showed reductions in populations of approximately 55-75%, and also approximately 34-40% less matrix (proteoglycan) production as compared to parental and random control lines. Further, this reduction in matrix production was accompanied by significant downregulation of chondrogenic marker genes, such as Sox9, Collagen type II (Col II), and Collagen type X (Col X). Lastly, reintroduction of Mustn1 into a silenced cell line rescued this phenotype, returning proliferation rate, matrix production, and chondrogenic marker gene expression back to parental levels. Taken together these data suggest that Mustn1 is a necessary regulator of chondrocyte function.

Dataset Information

Schematic memories develop quickly, but are not expressed unless necessary.

Publications

Schematic memories develop quickly, but are not expressed unless necessary.

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