Transcriptional reprogramming at the intersection of the heat shock response and proteostasis
Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to prote...
Uloženo v:
| Vydáno v: | Molecular cell Ročník 84; číslo 1; s. 80 |
|---|---|
| Hlavní autoři: | , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
United States
04.01.2024
|
| Témata: | |
| ISSN: | 1097-4164, 1097-4164 |
| On-line přístup: | Zjistit podrobnosti o přístupu |
| Tagy: |
Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
|
| Abstract | Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to proteotoxic stress. The HSR encompasses a dual regulation of transcription, characterized by rapid activation of genes encoding molecular chaperones and concomitant global attenuation of non-chaperone genes. Recent genome-wide approaches have delineated the molecular depth of stress-induced transcriptional reprogramming. The dramatic rewiring of gene and enhancer networks is driven by key transcription factors, including heat shock factors (HSFs), that together with chromatin-modifying enzymes remodel the 3D chromatin architecture, determining the selection of either gene activation or repression. Here, we highlight the current advancements of molecular mechanisms driving transcriptional reprogramming during acute heat stress. We also discuss the emerging implications of HSF-mediated stress signaling in the context of physiological and pathological conditions. |
|---|---|
| AbstractList | Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to proteotoxic stress. The HSR encompasses a dual regulation of transcription, characterized by rapid activation of genes encoding molecular chaperones and concomitant global attenuation of non-chaperone genes. Recent genome-wide approaches have delineated the molecular depth of stress-induced transcriptional reprogramming. The dramatic rewiring of gene and enhancer networks is driven by key transcription factors, including heat shock factors (HSFs), that together with chromatin-modifying enzymes remodel the 3D chromatin architecture, determining the selection of either gene activation or repression. Here, we highlight the current advancements of molecular mechanisms driving transcriptional reprogramming during acute heat stress. We also discuss the emerging implications of HSF-mediated stress signaling in the context of physiological and pathological conditions.Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to proteotoxic stress. The HSR encompasses a dual regulation of transcription, characterized by rapid activation of genes encoding molecular chaperones and concomitant global attenuation of non-chaperone genes. Recent genome-wide approaches have delineated the molecular depth of stress-induced transcriptional reprogramming. The dramatic rewiring of gene and enhancer networks is driven by key transcription factors, including heat shock factors (HSFs), that together with chromatin-modifying enzymes remodel the 3D chromatin architecture, determining the selection of either gene activation or repression. Here, we highlight the current advancements of molecular mechanisms driving transcriptional reprogramming during acute heat stress. We also discuss the emerging implications of HSF-mediated stress signaling in the context of physiological and pathological conditions. Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient survival programs. The heat shock response (HSR) is an evolutionarily well-conserved survival program that is activated in response to proteotoxic stress. The HSR encompasses a dual regulation of transcription, characterized by rapid activation of genes encoding molecular chaperones and concomitant global attenuation of non-chaperone genes. Recent genome-wide approaches have delineated the molecular depth of stress-induced transcriptional reprogramming. The dramatic rewiring of gene and enhancer networks is driven by key transcription factors, including heat shock factors (HSFs), that together with chromatin-modifying enzymes remodel the 3D chromatin architecture, determining the selection of either gene activation or repression. Here, we highlight the current advancements of molecular mechanisms driving transcriptional reprogramming during acute heat stress. We also discuss the emerging implications of HSF-mediated stress signaling in the context of physiological and pathological conditions. |
| Author | Sistonen, Lea Pessa, Jenny C Joutsen, Jenny |
| Author_xml | – sequence: 1 givenname: Jenny C surname: Pessa fullname: Pessa, Jenny C organization: Faculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland; Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland – sequence: 2 givenname: Jenny surname: Joutsen fullname: Joutsen, Jenny organization: Department of Pathology, Lapland Central Hospital, Lapland Wellbeing Services County, Rovaniemi, Finland – sequence: 3 givenname: Lea surname: Sistonen fullname: Sistonen, Lea email: lea.sistonen@abo.fi organization: Faculty of Science and Engineering, Cell Biology, Åbo Akademi University, Turku, Finland; Turku Bioscience Centre, University of Turku and Åbo Akademi University, Turku, Finland. Electronic address: lea.sistonen@abo.fi |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38103561$$D View this record in MEDLINE/PubMed |
| BookMark | eNpNkMtOwzAQRS1URB_wBwhlySZh_EiaLFFFAakSm7JEkeNMWpfEDra74O8xUCRWM5o5d-7ozsnEWIOEXFPIKNDi7pANtlfYZwwYzyjNgIkzMqNQLVNBCzH510_J3PsDABV5WV2QKS8p8LygM_K2ddJ45fQYtDWyTxyOzu6cHAZtdokMSdhjok1A51F9M4ntfmZ7jEu_t-o9avxojcdEmjaJ8oDWB-m1vyTnnew9Xp3qgryuH7arp3Tz8vi8ut-kSggaUuR5jg2ggLZhqoWOylbJZSMZj_-CQlmwosK2qUCWjJeiA5ZzVXZLqKoub9iC3P7ejeYfR_ShHrSP2fTSoD36mlXAOStoCRG9OaHHZsC2Hp0epPus_yJhXzaPaOQ |
| CitedBy_id | crossref_primary_10_1111_acel_70038 crossref_primary_10_1016_j_cstres_2024_03_001 crossref_primary_10_3390_ijms26072843 crossref_primary_10_1038_s41598_025_08735_3 crossref_primary_10_1038_s44318_024_00234_x crossref_primary_10_1016_j_jbc_2025_110511 crossref_primary_10_1093_genetics_iyaf042 crossref_primary_10_3390_ijms26031057 crossref_primary_10_1016_j_envexpbot_2025_106192 crossref_primary_10_1016_j_pbi_2024_102590 crossref_primary_10_1016_j_celrep_2025_116227 crossref_primary_10_1111_pce_70062 crossref_primary_10_1371_journal_ppat_1013108 crossref_primary_10_1126_sciadv_ady1289 crossref_primary_10_1002_bit_70050 crossref_primary_10_1038_s41597_025_05557_w crossref_primary_10_1016_j_phrs_2024_107355 crossref_primary_10_1016_j_cell_2025_03_025 crossref_primary_10_1091_mbc_E25_01_0027 crossref_primary_10_1016_j_nantod_2025_102838 crossref_primary_10_1002_mco2_736 crossref_primary_10_3390_cells14030204 crossref_primary_10_1111_febs_70139 crossref_primary_10_1016_j_cstres_2024_01_006 crossref_primary_10_1083_jcb_202410205 |
| ContentType | Journal Article |
| Copyright | Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved. |
| Copyright_xml | – notice: Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved. |
| DBID | NPM 7X8 |
| DOI | 10.1016/j.molcel.2023.11.024 |
| DatabaseName | PubMed MEDLINE - Academic |
| DatabaseTitle | PubMed MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic PubMed |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: 7X8 name: MEDLINE - Academic url: https://search.proquest.com/medline sourceTypes: Aggregation Database |
| DeliveryMethod | no_fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1097-4164 |
| ExternalDocumentID | 38103561 |
| Genre | Journal Article Review |
| GroupedDBID | --- --K -DZ -~X 0R~ 123 1~5 2WC 4.4 457 4G. 5RE 62- 7-5 AAEDT AAEDW AAHBH AAKRW AAKUH AALRI AAMRU AAVLU AAXUO AAYWO ABDGV ABJNI ABMAC ACGFO ACGFS ACNCT ACVFH ADBBV ADCNI ADEZE AEFWE AENEX AEUPX AEXQZ AFFNX AFPUW AFTJW AGCQF AGKMS AIGII AITUG AKAPO AKBMS AKRWK AKYEP ALMA_UNASSIGNED_HOLDINGS AMRAJ APXCP ASPBG AVWKF AZFZN BAWUL CS3 DIK DU5 E3Z EBS EFKBS F5P FCP FDB FEDTE FIRID HH5 HVGLF IH2 IHE IXB J1W JIG KQ8 L7B M3Z M41 N9A NPM O-L O9- OK1 P2P ROL RPZ SDG SES SSZ TR2 7X8 |
| ID | FETCH-LOGICAL-c441t-e355eb0e40db2cd0f1adca7ba235890cea6269edb90a82384f0253c8f7099f5b2 |
| IEDL.DBID | 7X8 |
| ISICitedReferencesCount | 33 |
| ISICitedReferencesURI | http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=001154345200001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| ISSN | 1097-4164 |
| IngestDate | Sun Sep 28 10:00:47 EDT 2025 Mon Jul 21 05:58:51 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | transcription factor Pol II enhancer transcription HSR PTM post-translational modification chromatin proteostasis heat shock factor HSF heat shock response RNA polymerase II |
| Language | English |
| License | Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c441t-e355eb0e40db2cd0f1adca7ba235890cea6269edb90a82384f0253c8f7099f5b2 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
| OpenAccessLink | https://dx.doi.org/10.1016/j.molcel.2023.11.024 |
| PMID | 38103561 |
| PQID | 2903326180 |
| PQPubID | 23479 |
| ParticipantIDs | proquest_miscellaneous_2903326180 pubmed_primary_38103561 |
| PublicationCentury | 2000 |
| PublicationDate | 2024-01-04 |
| PublicationDateYYYYMMDD | 2024-01-04 |
| PublicationDate_xml | – month: 01 year: 2024 text: 2024-01-04 day: 04 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Molecular cell |
| PublicationTitleAlternate | Mol Cell |
| PublicationYear | 2024 |
| SSID | ssj0014589 |
| Score | 2.57131 |
| SecondaryResourceType | review_article |
| Snippet | Cellular homeostasis is constantly challenged by a myriad of extrinsic and intrinsic stressors. To mitigate the stress-induced damage, cells activate transient... |
| SourceID | proquest pubmed |
| SourceType | Aggregation Database Index Database |
| StartPage | 80 |
| Title | Transcriptional reprogramming at the intersection of the heat shock response and proteostasis |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/38103561 https://www.proquest.com/docview/2903326180 |
| Volume | 84 |
| WOSCitedRecordID | wos001154345200001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D |
| hasFullText | |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LS8QwEA7qKnjx_VhfRPAaTZt0255ExMWDLntQ2IuUdJLgwm67blfBf-8kbdmTIEihh5KUMpnOfMnMfEPIlbBgAg6KSSuAoT9WLE24Zs63CWFSvDxl_lM8GCSjUTpsDtyqJq2ytYneUOsS3Bn5TZhygVAjSPjt7IO5rlEuutq00FglHYFQxqV0xaNlFEFGvgWeC7IyBB6yLZ3z-V3TcgLGBR9Cce14PF3N-28g0zub_vZ_P3OHbDUwk97VerFLVkyxRzbqxpPf--TNu6jWYOBAx23pE7Wm6MqoWlDEhdRRScwrn6tV0NL6Z8520-odrSjO8em1hqpCU8_3UCLUrMbVAXntP7zcP7Km0QIDREMLZnBhTM6N5DoPQXMbKA0qzpWro005GIXbntToPOUqQR8vLSIlAYmNEV_aKA8PyVpRFuaYUK4TxU0EYHGjImN8ayKlCiIINAjo9brkspVbhorsohOqMOVnlS0l1yVHtfCzWc24kTkaMoFI7-QPs0_JJq6p9Mck8ox0LP7G5pysw9diXM0vvIbgfTB8_gGGFsfQ |
| linkProvider | ProQuest |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Transcriptional+reprogramming+at+the+intersection+of+the+heat+shock+response+and+proteostasis&rft.jtitle=Molecular+cell&rft.au=Pessa%2C+Jenny+C&rft.au=Joutsen%2C+Jenny&rft.au=Sistonen%2C+Lea&rft.date=2024-01-04&rft.issn=1097-4164&rft.eissn=1097-4164&rft.volume=84&rft.issue=1&rft.spage=80&rft_id=info:doi/10.1016%2Fj.molcel.2023.11.024&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1097-4164&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1097-4164&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1097-4164&client=summon |