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SQUAMOSA Promoter-Binding Transcription Factors: A New Mechanism in Plant Cell Death Regulation
SQUAMOSA Promoter-Binding Transcription Factors: A New Mechanism in Plant Cell Death Regul...
SQUAMOSA Promoter-Binding Transcription Factors: A New Mechanism in Plant Cell Death Regulation

상세정보

자료유형  
 학위논문 서양
최종처리일시  
20260202105257
ISBN  
9798297957671
DDC  
581
저자명  
VanDenTop, Austin.
서명/저자  
SQUAMOSA Promoter-Binding Transcription Factors: A New Mechanism in Plant Cell Death Regulation
발행사항  
[Sl] : The University of Wisconsin - Madison, 2025
발행사항  
Ann Arbor : ProQuest Dissertations & Theses, 2025
형태사항  
147 p
주기사항  
Source: Dissertations Abstracts International, Volume: 87-04, Section: B.
주기사항  
Advisor: Kabbage, Mehdi.
학위논문주기  
Thesis (Ph.D.)--The University of Wisconsin - Madison, 2025.
초록/해제  
요약Programmed cell death (PCD) is a core biological process that shapes nearly every aspect of plant life, from developmental transitions to responses against abiotic and biotic insults. Selective dismantling of cells underpins key survival strategies, such tissue differentiation and responses to pathogens. Despite its importance, the molecular basis of plant PCD remains poorly defined. Although PCD in plants shares morphological hallmarks with animal apoptosis, the core apoptotic regulators of animals are absent from plant genomes. Instead, plants rely on largely unknown mechanisms for PCD induction. Addressing this gap is critical both for advancing mechanistic understanding and for uncovering targets to improve crop resilience.This work establishes a conserved clade of SQUAMOSA promoter-binding protein (SBP-box) transcription factors as key regulators of stress-induced PCD. Tomato SlySBP12a and its Arabidopsis homologs AtSPL1 and AtSPL12 contain conserved C-terminal transmembrane domains (TMDs) that tether them to the endoplasmic reticulum (ER) membrane. Under basal conditions, the transcription factors are sequestered on the ER membrane; under ER stress, the proteins relocalize to the nucleus and activate pro-death transcriptional programs. Their activity is further tuned by the E3 ligase SINAT2, which promotes proteasomal degradation, providing dual regulation through both localization and turnover.Transcriptomic profiling of Nicotiana benthamiana leaves expressing tomato SlySBP8b and SlySBP12a revealed strong induction of proteases, providing a direct mechanistic link to PCD execution. Functional assays confirmed that several proteases triggered moderate cell death when expressed individually, and ion leakage assays supported their role in disrupting membrane integrity. These included cathepsin- and subtilisin-like proteases with established caspase-like activity in plants, underscoring conserved biochemical strategies of protease-mediated dismantling. Together, these results demonstrate that SBP-box proteins act as upstream switches that directly engage proteolytic machinery to promote programmed cell death.Beyond their shared induction of proteases, SlySBP8b and SlySBP12a diverged in the specific stress programs they activated. SlySBP8b upregulated immune-associated genes, including defensins, resistance (R) genes, and a 4-coumarate-CoA ligase linked to antimicrobial phenolic intermediates. In contrast, SlySBP12a preferentially activated structural defense pathways such as phenylpropanoid biosynthesis, lignin polymerization, and very long-chain fatty acid elongation, which contribute to wall fortification and membrane stability. Promoter analyses revealed SBP-binding motifs across these gene sets, supporting direct regulation. These models suggest that SBPs act at the interface of stress survival and cell death, shaping transcriptional responses that can serve both protective and sacrificial functions.Finally, evolutionary analyses showed that the clade containing SlySBP12a and AtSPL1/12 is consistently marked by conserved C-terminal TMDs across monocots and dicots, suggesting ER tethering and stress-induced release is a conserved strategy. This conservation highlights SBP-box transcription factors as an entry point for manipulating PCD across diverse crops. Importantly, downstream genes regulated by SlySBP12a, together with regulatory models like SINAT2, identify tractable points of intervention for tuning PCD. Targeted manipulation of these pathways could provide new strategies for engineering stress resilience, enhancing tolerance to environmental challenges such as heat, salinity, drought, and pathogen attack.
일반주제명  
Plant pathology
일반주제명  
Molecular biology
일반주제명  
Plant sciences
일반주제명  
Cellular biology
키워드  
Cell biology
키워드  
Plant genetics
키워드  
Programmed cell death
키워드  
Transcription factors
기타저자  
The University of Wisconsin - Madison Plant Pathology
기본자료저록  
Dissertations Abstracts International. 87-04B.
전자적 위치 및 접속  
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MARC

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■040    ▼aMiAaPQ▼cMiAaPQ
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■1001  ▼aVanDenTop,  Austin.
■24510▼aSQUAMOSA  Promoter-Binding  Transcription  Factors:  A  New  Mechanism  in  Plant  Cell  Death  Regulation
■260    ▼a[Sl]▼bThe  University  of  Wisconsin  -  Madison▼c2025
■260  1▼aAnn  Arbor▼bProQuest  Dissertations  &  Theses▼c2025
■300    ▼a147  p
■500    ▼aSource:  Dissertations  Abstracts  International,  Volume:  87-04,  Section:  B.
■500    ▼aAdvisor:  Kabbage,  Mehdi.
■5021  ▼aThesis  (Ph.D.)--The  University  of  Wisconsin  -  Madison,  2025.
■520    ▼aProgrammed  cell  death  (PCD)  is  a  core  biological  process  that  shapes  nearly  every  aspect  of  plant  life,  from  developmental  transitions  to  responses  against  abiotic  and  biotic  insults.  Selective  dismantling  of  cells  underpins  key  survival  strategies,  such  tissue  differentiation  and  responses  to  pathogens.  Despite  its  importance,  the  molecular  basis  of  plant  PCD  remains  poorly  defined.  Although  PCD  in  plants  shares  morphological  hallmarks  with  animal  apoptosis,  the  core  apoptotic  regulators  of  animals  are  absent  from  plant  genomes.  Instead,  plants  rely  on  largely  unknown  mechanisms  for  PCD  induction.  Addressing  this  gap  is  critical  both  for  advancing  mechanistic  understanding  and  for  uncovering  targets  to  improve  crop  resilience.This  work  establishes  a  conserved  clade  of  SQUAMOSA  promoter-binding  protein  (SBP-box)  transcription  factors  as  key  regulators  of  stress-induced  PCD.  Tomato  SlySBP12a  and  its  Arabidopsis  homologs  AtSPL1  and  AtSPL12  contain  conserved  C-terminal  transmembrane  domains  (TMDs)  that  tether  them  to  the  endoplasmic  reticulum  (ER)  membrane.  Under  basal  conditions,  the  transcription  factors  are  sequestered  on  the  ER  membrane;  under  ER  stress,  the  proteins  relocalize  to  the  nucleus  and  activate  pro-death  transcriptional  programs.  Their  activity  is  further  tuned  by  the  E3  ligase  SINAT2,  which  promotes  proteasomal  degradation,  providing  dual  regulation  through  both  localization  and  turnover.Transcriptomic  profiling  of  Nicotiana  benthamiana  leaves  expressing  tomato  SlySBP8b  and  SlySBP12a  revealed  strong  induction  of  proteases,  providing  a  direct  mechanistic  link  to  PCD  execution.  Functional  assays  confirmed  that  several  proteases  triggered  moderate  cell  death  when  expressed  individually,  and  ion  leakage  assays  supported  their  role  in  disrupting  membrane  integrity.  These  included  cathepsin-  and  subtilisin-like  proteases  with  established  caspase-like  activity  in  plants,  underscoring  conserved  biochemical  strategies  of  protease-mediated  dismantling.  Together,  these  results  demonstrate  that  SBP-box  proteins  act  as  upstream  switches  that  directly  engage  proteolytic  machinery  to  promote  programmed  cell  death.Beyond  their  shared  induction  of  proteases,  SlySBP8b  and  SlySBP12a  diverged  in  the  specific  stress  programs  they  activated.  SlySBP8b  upregulated  immune-associated  genes,  including  defensins,  resistance  (R)  genes,  and  a  4-coumarate-CoA  ligase  linked  to  antimicrobial  phenolic  intermediates.  In  contrast,  SlySBP12a  preferentially  activated  structural  defense  pathways  such  as  phenylpropanoid  biosynthesis,  lignin  polymerization,  and  very  long-chain  fatty  acid  elongation,  which  contribute  to  wall  fortification  and  membrane  stability.  Promoter  analyses  revealed  SBP-binding  motifs  across  these  gene  sets,  supporting  direct  regulation.  These  models  suggest  that  SBPs  act  at  the  interface  of  stress  survival  and  cell  death,  shaping  transcriptional  responses  that  can  serve  both  protective  and  sacrificial  functions.Finally,  evolutionary  analyses  showed  that  the  clade  containing  SlySBP12a  and  AtSPL1/12  is  consistently  marked  by  conserved  C-terminal  TMDs  across  monocots  and  dicots,  suggesting  ER  tethering  and  stress-induced  release  is  a  conserved  strategy.  This  conservation  highlights  SBP-box  transcription  factors  as  an  entry  point  for  manipulating  PCD  across  diverse  crops.  Importantly,  downstream  genes  regulated  by  SlySBP12a,  together  with  regulatory  models  like  SINAT2,  identify  tractable  points  of  intervention  for  tuning  PCD.  Targeted  manipulation  of  these  pathways  could  provide  new  strategies  for  engineering  stress  resilience,  enhancing  tolerance  to  environmental  challenges  such  as  heat,  salinity,  drought,  and  pathogen  attack.
■590    ▼aSchool  code:  0262.
■650  4▼aPlant  pathology
■650  4▼aMolecular  biology
■650  4▼aPlant  sciences
■650  4▼aCellular  biology
■653    ▼aCell  biology
■653    ▼aPlant  genetics
■653    ▼aProgrammed  cell  death
■653    ▼aTranscription  factors
■690    ▼a0480
■690    ▼a0307
■690    ▼a0479
■690    ▼a0379
■71020▼aThe  University  of  Wisconsin  -  Madison▼bPlant  Pathology.
■7730  ▼tDissertations  Abstracts  International▼g87-04B.
■790    ▼a0262
■791    ▼aPh.D.
■792    ▼a2025
■793    ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17360054▼nKERIS▼z이  자료의  원문은  한국교육학술정보원에서  제공합니다.

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