Salvato in:
Dettagli Bibliografici
Autori principali: Majerová, Eva, Steinle, Camryn, Drury, Crawford
Natura: Artículo científico
Lingua:en
Pubblicazione: Communications biology 2025
Soggetti:
Accesso online:https://pubmed.ncbi.nlm.nih.gov/40804160/
Tags: Aggiungi Tag
Nessun Tag, puoi essere il primo ad aggiungerne!!
_version_ 1868266165165359105
author Majerová, Eva
Steinle, Camryn
Drury, Crawford
author_facet Majerová, Eva
Steinle, Camryn
Drury, Crawford
Majerová, Eva
Steinle, Camryn
Drury, Crawford
collection PubMed - marine biology
contents BAK knockdown delays bleaching and alleviates oxidative DNA damage in a reef-building coral. Majerová, Eva Steinle, Camryn Drury, Crawford Animals Anthozoa Coral Reefs DNA Damage Symbiosis Oxidative Stress Coral Bleaching Climate Change Gene Knockdown Techniques Heat-Shock Response As climate change threatens marine ecosystems, efforts to restore coral reefs using resilient corals are increasing. This conservation approach remains limited by our understanding of cellular mechanisms of resilience and trade-offs. Here, we demonstrate that downregulation of pa-BAK stabilizes the coral-algal endosymbiosis and slows bleaching during acute heat stress in Pocillopora acuta through coordinated expression of gene clusters. The improvement in thermal tolerance was closely related to the downregulation efficiency in individual corals. Oxidative DNA damage, a hallmark of thermal stress response, was prevented in corals with stabilized symbiosis, likely through a decrease in mitochondrial ROS release. We hypothesize that this manipulation causes a cascading molecular response, which may impact other traits such as oxidative mitochondrial damage, proving detrimental over the longer term. Developing our understanding of heat-stress defense mechanisms that promote stability in the coral-algal symbiosis is fundamental for effective modern coral reef restoration practices based on improving ecosystem resilience.
format Artículo científico
id pubmed_40804160
institution PubMed
language en
publishDate 2025
publisher Communications biology
record_format pubmed
spellingShingle BAK knockdown delays bleaching and alleviates oxidative DNA damage in a reef-building coral.
Majerová, Eva
Steinle, Camryn
Drury, Crawford
Animals
Anthozoa
Coral Reefs
DNA Damage
Symbiosis
Oxidative Stress
Coral Bleaching
Climate Change
Gene Knockdown Techniques
Heat-Shock Response
BAK knockdown delays bleaching and alleviates oxidative DNA damage in a reef-building coral. Majerová, Eva Steinle, Camryn Drury, Crawford Animals Anthozoa Coral Reefs DNA Damage Symbiosis Oxidative Stress Coral Bleaching Climate Change Gene Knockdown Techniques Heat-Shock Response As climate change threatens marine ecosystems, efforts to restore coral reefs using resilient corals are increasing. This conservation approach remains limited by our understanding of cellular mechanisms of resilience and trade-offs. Here, we demonstrate that downregulation of pa-BAK stabilizes the coral-algal endosymbiosis and slows bleaching during acute heat stress in Pocillopora acuta through coordinated expression of gene clusters. The improvement in thermal tolerance was closely related to the downregulation efficiency in individual corals. Oxidative DNA damage, a hallmark of thermal stress response, was prevented in corals with stabilized symbiosis, likely through a decrease in mitochondrial ROS release. We hypothesize that this manipulation causes a cascading molecular response, which may impact other traits such as oxidative mitochondrial damage, proving detrimental over the longer term. Developing our understanding of heat-stress defense mechanisms that promote stability in the coral-algal symbiosis is fundamental for effective modern coral reef restoration practices based on improving ecosystem resilience.
title BAK knockdown delays bleaching and alleviates oxidative DNA damage in a reef-building coral.
topic Animals
Anthozoa
Coral Reefs
DNA Damage
Symbiosis
Oxidative Stress
Coral Bleaching
Climate Change
Gene Knockdown Techniques
Heat-Shock Response
url https://pubmed.ncbi.nlm.nih.gov/40804160/