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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 Regulation
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202105257
- ISBN
- 9798297957671
- DDC
- 581
- 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
- 기타저자
- The University of Wisconsin - Madison Plant Pathology
- 기본자료저록
- Dissertations Abstracts International. 87-04B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■020 ▼a9798297957671
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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.


