@article{PAR00009921,
  title = {{R}egulation of {A}poptotic {M}ediators {R}eveals {D}ynamic {R}esponses to {T}hermal {S}tress in the {R}eef {B}uilding {C}oral {A}cropora millepora},
  author = {{P}ernice, {M}. and {D}unn, {S}. {R}. and {M}iard, {T}. and {D}ufour, {S}ylvie and {D}ove, {S}. and {H}oegh-{G}uldberg, {O}.},
  editor = {},
  language = {{ENG}},
  abstract = {{B}ackground: {M}ass coral bleaching is increasing in scale and frequency across the world's coral reefs and is being driven primarily by increased levels of thermal stress arising from global warming. {I}n order to understand the impacts of projected climate change upon corals reefs, it is important to elucidate the underlying cellular mechanisms that operate during coral bleaching and subsequent mortality. {I}n this respect, increased apoptotic cell death activity is an important cellular process that is associated with the breakdown of the mutualistic symbiosis between the cnidarian host and their dinoflagellate symbionts. {M}ethodology/{P}rincipal {F}indings: {T}he present study reports the impacts of different stressors (colchicine and heat stress) on three phases of apoptosis: (i) the potential initiation by differential expression of {B}cl-2 members, (ii) the execution of apoptotic events by activation of caspase 3-like proteases and (iii) and finally, the cell disposal indicated by {DNA} fragmentation in the reef building coral {A}cropora millepora. {I}n corals incubated with colchicine, an increase in caspase 3-like activity and {DNA} fragmentation was associated with a relative down-regulation of {B}cl-2, suggesting that the initiation of apoptosis may be mediated by the suppression of an anti-apoptotic mechanism. {I}n contrast, in the early steps of heat stress, the induction of caspase-dependent apoptosis was related to a relative up-regulation of {B}cl-2 consecutively followed by a delayed decrease in apoptosis activity. {C}onclusions/{S}ignificance: {I}n the light of these results, we propose a model of heat stress in coral hosts whereby increasing temperatures engage activation of caspase 3-dependent apoptosis in cells designated for termination, but also the onset of a delayed protective response involving overexpression of {B}cl-2 in surviving cells. {T}his mitigating response to thermal stress could conceivably be an important regulatory mechanism for cell survival in corals exposed to sudden environmental changes.},
  keywords = {},
  booktitle = {},
  journal = {{P}los {O}ne},
  volume = {6},
  numero = {1},
  pages = {e16095},
  ISSN = {1932-6203},
  year = {2011},
  DOI = {10.1371/journal.pone.0016095},
  URL = {https://www.documentation.ird.fr/hor/{PAR}00009921},
}