Conserved modulation of the constitutive photomorphogenic 1 E3 ubiquitin ligase activity by the bHLH transcription factors, phytochrome interacting factors

dc.contributor.advisorHuq, Enamul
dc.contributor.committeeMemberRoux, Stanley J
dc.contributor.committeeMemberVokes, Steven A
dc.contributor.committeeMemberLloyd, Alan M
dc.contributor.committeeMemberLinder, Craig R
dc.creatorXu, Xiaosa
dc.creator.orcid0000-0002-3452-6751
dc.date.accessioned2016-09-06T19:41:58Z
dc.date.available2016-09-06T19:41:58Z
dc.date.issued2016-05
dc.date.submittedMay 2016
dc.date.updated2016-09-06T19:41:58Z
dc.description.abstractAs sessile organism, plants are informed of the time of the day and their place of growth by a collection of photoreceptors that detect changing intensity, quality, and direction of light in the environment. Among these photoreceptors, phytochromes (A, B, C, D, E) are the major ones to drive a developmental switch for initial emergence of seedlings from subterranean darkness into sunlight, called plant photomorphogenesis. Previous studies have identified many regulators in the phytochorme-mediated photomorphogenesis pathway. Among them, CONSTITUTIVELY PHOTOMORPHOGENIC 1/ SUPPRESSOR OF PHYTOCHROME A (COP1/SPA) complex and PHYTOCHROME INTERACTING FACTORs (PIF1, 3, 4, 5, 7, 8) are key negative regulators that can suppress photomorphogenesis individually. However, the functional relationships between the COP1-SPA and the PIFs are still unknown. Here in my dissertation project, I showed that PIFs have nontranscriptional roles by acting as cofactors of the COP1 E3 Ubiquitin ligase to enhance the trans-ubiquitination and subsequent degradation of the substrates of COP1, including LONG HYPOCOTYL 5 (HY5), LONG HYPOCOTYL IN FAR-RED 1 (HFR1) and a newly identified substrate HECATE 2 (HEC2), to suppress photomorphogenesis. HFR1 also promotes the degradation of PIF1 in the dark via direct heterodimerization to trigger rapid seed germination upon light exposure. The reciprocal co-degradation between PIF1 and HFR1 is dependent on the ubi/26S-proteasome pathway in vivo. In addition, the cop1 and pif1, 3, 4, 5 mutant combinations showed overproliferation of stigmatic tissues phenotype similar to HEC overexpression plants. Biochemical and genetic evidence showed that HECs are highly abundant in the cop1 pifs mutant flowers. Moreover, HECs negatively regulate the PIFs’ binding activity to the G-box regions of promoters of flower pattern genes, SEP1 and SEP3. Taken together, these data revealed the conserved modulation of the COP1 Ubiquitin E3 ligase activity by PIFs, uncovered a suicidal co-degradation mechanism between the HFR1 and PIF1 to fine tune seed germination and seedling development, and demonstrated a novel function of COP1 and PIFs in regulating flower pattern development.
dc.description.departmentPlant Biology
dc.format.mimetypeapplication/pdf
dc.identifierdoi:10.15781/T2P55DH50
dc.identifier.urihttp://hdl.handle.net/2152/40247
dc.language.isoen
dc.subjectArabidopsis
dc.subjectPhotomorphogenesis
dc.subjectCOP1-SPA complexes
dc.subjectPhytochrome interacting factors
dc.subjectHLH transcription factor (HFR1)
dc.subjectUbiquitin-26S proteasome
dc.subjectSuicidal co-degradation
dc.subjectHLH transcription factors (HECATEs)
dc.subjectFlower pattern development
dc.titleConserved modulation of the constitutive photomorphogenic 1 E3 ubiquitin ligase activity by the bHLH transcription factors, phytochrome interacting factors
dc.typeThesis
dc.type.materialtext
thesis.degree.departmentPlant Biology
thesis.degree.disciplinePlant biology
thesis.degree.grantorThe University of Texas at Austin
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy

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