LIP1 Regulates the Plant Circadian Oscillator by Modulating the Function of the Clock Component GIGANTEA

Author:

Hajdu Anita123,Nyári Dóra124,Terecskei Kata2,Gyula Péter5ORCID,Ádám Éva23,Dobos Orsolya2,Mérai Zsuzsanna6ORCID,Kozma-Bognár László12ORCID

Affiliation:

1. Department of Genetics, Faculty of Sciences and Informatics, University of Szeged, H-6726 Szeged, Hungary

2. Institute of Plant Biology, HUN-REN Biological Research Centre, H-6726 Szeged, Hungary

3. Department of Medical Genetics, Faculty of Medicine, University of Szeged, H-6720 Szeged, Hungary

4. Doctoral School in Biology, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary

5. Institute of Genetics and Biotechnology, Hungarian University of Agriculture and Life Sciences, H-2100 Gödöllő, Hungary

6. Gregor Mendel Institute of Molecular Plant Biology GmbH, 1030 Vienna, Austria

Abstract

Circadian clocks are biochemical timers regulating many physiological and molecular processes according to the day/night cycles. The function of the oscillator relies on negative transcriptional/translational feedback loops operated by the so-called clock genes and the encoded clock proteins. Previously, we identified the small GTPase LIGHT INSENSITIVE PERIOD 1 (LIP1) as a circadian-clock-associated protein that regulates light input to the clock in the model plant Arabidopsis thaliana. We showed that LIP1 is also required for suppressing red and blue light-mediated photomorphogenesis, pavement cell shape determination and tolerance to salt stress. Here, we demonstrate that LIP1 is present in a complex of clock proteins GIGANTEA (GI), ZEITLUPE (ZTL) and TIMING OF CAB 1 (TOC1). LIP1 participates in this complex via GUANINE EX-CHANGE FACTOR 7. Analysis of genetic interactions proved that LIP1 affects the oscillator via modulating the function of GI. We show that LIP1 and GI independently and additively regulate photomorphogenesis and salt stress responses, whereas controlling cell shape and photoperiodic flowering are not shared functions of LIP1 and GI. Collectively, our results suggest that LIP1 affects a specific function of GI, possibly by altering binding of GI to downstream signalling components.

Funder

NATIONAL RESEARCH, DEVELOPMENT AND INNOVATION OFFICE

HUNGARIAN ACADEMY OF SCIENCES

AUSTRIAN SCIENCE FUND

Publisher

MDPI AG

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