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Projekt Druckansicht

Genetische Analyse von Signalwegen in Reaktion auf erhöhte Umgebungstemperaturen in Arabidopsis thaliana

Fachliche Zuordnung Pflanzenphysiologie
Genetik und Genomik der Pflanzen
Förderung Förderung von 2012 bis 2024
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 223862977
 
Erstellungsjahr 2022

Zusammenfassung der Projektergebnisse

This project aimed to identify novel regulators that mediate morphological plant responses to warm temperatures (termed thermomorphogenesis) and to characterize their function within the known framework of molecular regulators that centers around the transcription factor PIF4. Using a forward genetic approach, we previously have isolated mutants which are compromised in their ability to elongate hypocotyls in response to elevated temperatures. Identification of the genes that cause the altered phenotype resulted in two promising candidates: D6PK and SMAX1. While SMAX1 function in thermomorphogenesis has recently been published by another group, we were able to show that D6PK is required for temperature-induced auxin to translocate from cotyledons into the hypocotyl to induce cell elongation. In a second approach, we aimed to specifically identify transcription factors that contribute to thermomorphogenesis regulation using the available TRANSPLANTA collection which allows inducible overexpression of hundreds of transcription factor genes. Here, several promising candidate genes were identified that caused hypersensitive or reduced temperature responses. While characterization of their potential role in thermomrophogenesis is ongoing for several of the identified TFs, we focused specifically on a group of (b)HLH transcription factors, some of which have previously been implicated as regulators of cell elongation. For several members of this TF family, a tripartite level of antagonistic regulation has been implicated in response to several stimuli. This tri-antagonistic system involves the actual bHLH transcriptional regulators which can be repressed by binding to a HLH repressor. The repressor can be scavenged by binding of a secondary HLH repressor which thereby de-represses the inhibition of the actual transcriptional regulator. We were able to show that PIF4 function at warm ambient temperature can be modulated by PAR repressors and PRE secondary repressors and that loss of the respective genes affects thermomorphogenesis. Furthermore, PIF4 can bind to the promoter of its secondary repressor PRE1 which suggests a feed-forward regulation by which PIF4 can prevent its inhibition via PARs by inducing a secondary repressor (PREs) to scavenge the repressor (PARs).

Projektbezogene Publikationen (Auswahl)

 
 

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