scholarly journals Cell geometry, signal dampening, and a bimodal transcriptional response underlie the spatial precision of an ERK-mediated embryonic induction

2021 ◽  
Author(s):  
Géraldine Williaume ◽  
Sophie de Buyl ◽  
Cathy Sirour ◽  
Nicolas Haupaix ◽  
Rossana Bettoni ◽  
...  
Keyword(s):  
Transcriptional Response ◽  
Embryonic Induction ◽  
Cell Geometry ◽  
Signal Dampening

scholarly journals Compressive force induces reversible chromatin condensation and cell geometry–dependent transcriptional response

2018 ◽  
Vol 29 (25) ◽  
pp. 3039-3051 ◽  
Author(s):  
Karthik Damodaran ◽  
Saradha Venkatachalapathy ◽  
Farid Alisafaei ◽  
A. V. Radhakrishnan ◽  
Doorgesh Sharma Jokhun ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Chromatin Condensation ◽  
Compressive Force ◽  
Transcriptional Response ◽  
Quantitative Model ◽  
Mouse Fibroblast ◽  
Cell Geometry ◽  
Connective Tissues ◽  
Actomyosin Contractility ◽  
The Impact

Fibroblasts exhibit heterogeneous cell geometries in tissues and integrate both mechanical and biochemical signals in their local microenvironment to regulate genomic programs via chromatin remodelling. While in connective tissues fibroblasts experience tensile and compressive forces (CFs), the role of compressive forces in regulating cell behavior and, in particular, the impact of cell geometry in modulating transcriptional response to such extrinsic mechanical forces is unclear. Here we show that CF on geometrically well-defined mouse fibroblast cells reduces actomyosin contractility and shuttles histone deacetylase 3 (HDAC3) into the nucleus. HDAC3 then triggers an increase in the heterochromatin content by initiating removal of acetylation marks on the histone tails. This suggests that, in response to CF, fibroblasts condense their chromatin and enter into a transcriptionally less active and quiescent states as also revealed by transcriptome analysis. On removal of CF, the alteration in chromatin condensation was reversed. We also present a quantitative model linking CF-dependent changes in actomyosin contractility leading to chromatin condensation. Further, transcriptome analysis also revealed that the transcriptional response of cells to CF was geometry dependent. Collectively, our results suggest that CFs induce chromatin condensation and geometry-dependent differential transcriptional response in fibroblasts that allows maintenance of tissue homeostasis.

Registered Report: Transcriptional Analysis of Savings Memory Suggests Forgetting Is Due to Retrieval Failure

2020 ◽  
Author(s):  
Robert Calin-Jageman ◽  
Irina Calin-Jageman ◽  
Tania Rosiles ◽  
Melissa Nguyen ◽  
Annette Garcia ◽  
...  
Keyword(s):  
Memory Trace ◽  
Aplysia Californica ◽  
Transcriptional Response ◽  
Transcriptional Analysis ◽  
Retrieval Failure ◽  
Initial Learning ◽  
Rigorous Test ◽  
Stage 1 ◽  
Induced Changes

[[This is a Stage 2 Registered Report manuscript now accepted for publication at eNeuro. The accepted Stage 1 manuscript is posted here: https://psyarxiv.com/s7dft, and the pre-registration for the project is available here (https://osf.io/fqh8j, 9/11/2019). A link to the final Stage 2 manuscript will be posted after peer review and publication.]] There is fundamental debate about the nature of forgetting: some have argued that it represents the decay of the memory trace, others that the memory trace persists but becomes inaccessible due to retrieval failure. These different accounts of forgetting lead to different predictions about savings memory, the rapid re-learning of seemingly forgotten information. If forgetting is due to decay, then savings requires re-encoding and should thus involve the same mechanisms as initial learning. If forgetting is due to retrieval failure, then savings should be mechanistically distinct from encoding. In this registered report we conducted a pre-registered and rigorous test between these accounts of forgetting. Specifically, we used microarray to characterize the transcriptional correlates of a new memory (1 day after training), a forgotten memory (8 days after training), and a savings memory (8 days after training but with a reminder on day 7 to evoke a long-term savings memory) for sensitization in Aplysia californica (n = 8 samples/group). We found that the re-activation of sensitization during savings does not involve a substantial transcriptional response. Thus, savings is transcriptionally distinct relative to a newer (1-day old) memory, with no co-regulated transcripts, negligible similarity in regulation-ranked ordering of transcripts, and a negligible correlation in training-induced changes in gene expression (r = .04 95% CI [-.12, .20]). Overall, our results suggest that forgetting of sensitization memory represents retrieval failure.

Sign in / Sign up

Export Citation Format

Share Document