A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana

Inhye Lee, Kuglae Kim, Sumin Lee, Seungjun Lee, Eunjin Hwang, Kihye Shin, Dayoung Kim, Jungki Choi, Hyunmo Choi, Jeong Seok Cha, Hoyoung Kim, Rin A. Lee, Suyeong Jeong, Jeongsik Kim, Yumi Kim, Hong Gil Nam, Soon Ki Park, Hyun Soo Cho, Moon Soo Soh

Research output: Contribution to journalArticle

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Abstract

A smoke-derived compound, karrikin (KAR), and an endogenous but as yet unidentified KARRIKIN INSENSITIVE2 (KAI2) ligand (KL) have been identified as chemical cues in higher plants that impact on multiple aspects of growth and development. Genetic screening of light-signaling mutants in Arabidopsis thaliana has identified a mutant designated as ply2 (pleiotropic long hypocotyl2) that has pleiotropic light-response defects. In this study, we used positional cloning to identify the molecular lesion of ply2 as a missense mutation of KAI2/HYPOSENSITIVE TO LIGHT, which causes a single amino acid substitution, Ala219Val. Physiological analysis and genetic epistasis analysis with the KL-signaling components MORE AXILLARY GROWTH2 (MAX2) and SUPPRESSOR OF MAX2 1 suggested that the pleiotropic phenotypes of the ply2 mutant can be ascribed to a defect in KL-signaling. Molecular and biochemical analyses revealed that the mutant KAI2 ply2 protein is impaired in its ligand-binding activity. In support of this conclusion, X-ray crystallography studies suggested that the KAI2 ply2 mutation not only results in a narrowed entrance gate for the ligand but also alters the structural flexibility of the helical lid domains. We discuss the structural implications of the Ala219 residue with regard to ligand-specific binding and signaling of KAI2, together with potential functions of KL-signaling in the context of the light-regulatory network in Arabidopsis thaliana.

Original languageEnglish
Pages (from-to)3609-3623
Number of pages15
JournalJournal of experimental botany
Volume69
Issue number15
DOIs
Publication statusPublished - 2018 Jun 27

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Arabidopsis
Arabidopsis thaliana
Alleles
Ligands
alleles
Light
mutants
Genetic Epistasis
lesions (plant)
missense mutation
lids
X Ray Crystallography
epistasis
Genetic Testing
amino acid substitution
Missense Mutation
Amino Acid Substitution
smoke
ligands
Growth and Development

All Science Journal Classification (ASJC) codes

  • Physiology
  • Plant Science

Cite this

Lee, Inhye ; Kim, Kuglae ; Lee, Sumin ; Lee, Seungjun ; Hwang, Eunjin ; Shin, Kihye ; Kim, Dayoung ; Choi, Jungki ; Choi, Hyunmo ; Cha, Jeong Seok ; Kim, Hoyoung ; Lee, Rin A. ; Jeong, Suyeong ; Kim, Jeongsik ; Kim, Yumi ; Nam, Hong Gil ; Park, Soon Ki ; Cho, Hyun Soo ; Soh, Moon Soo. / A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana. In: Journal of experimental botany. 2018 ; Vol. 69, No. 15. pp. 3609-3623.
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title = "A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana",
abstract = "A smoke-derived compound, karrikin (KAR), and an endogenous but as yet unidentified KARRIKIN INSENSITIVE2 (KAI2) ligand (KL) have been identified as chemical cues in higher plants that impact on multiple aspects of growth and development. Genetic screening of light-signaling mutants in Arabidopsis thaliana has identified a mutant designated as ply2 (pleiotropic long hypocotyl2) that has pleiotropic light-response defects. In this study, we used positional cloning to identify the molecular lesion of ply2 as a missense mutation of KAI2/HYPOSENSITIVE TO LIGHT, which causes a single amino acid substitution, Ala219Val. Physiological analysis and genetic epistasis analysis with the KL-signaling components MORE AXILLARY GROWTH2 (MAX2) and SUPPRESSOR OF MAX2 1 suggested that the pleiotropic phenotypes of the ply2 mutant can be ascribed to a defect in KL-signaling. Molecular and biochemical analyses revealed that the mutant KAI2 ply2 protein is impaired in its ligand-binding activity. In support of this conclusion, X-ray crystallography studies suggested that the KAI2 ply2 mutation not only results in a narrowed entrance gate for the ligand but also alters the structural flexibility of the helical lid domains. We discuss the structural implications of the Ala219 residue with regard to ligand-specific binding and signaling of KAI2, together with potential functions of KL-signaling in the context of the light-regulatory network in Arabidopsis thaliana.",
author = "Inhye Lee and Kuglae Kim and Sumin Lee and Seungjun Lee and Eunjin Hwang and Kihye Shin and Dayoung Kim and Jungki Choi and Hyunmo Choi and Cha, {Jeong Seok} and Hoyoung Kim and Lee, {Rin A.} and Suyeong Jeong and Jeongsik Kim and Yumi Kim and Nam, {Hong Gil} and Park, {Soon Ki} and Cho, {Hyun Soo} and Soh, {Moon Soo}",
year = "2018",
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Lee, I, Kim, K, Lee, S, Lee, S, Hwang, E, Shin, K, Kim, D, Choi, J, Choi, H, Cha, JS, Kim, H, Lee, RA, Jeong, S, Kim, J, Kim, Y, Nam, HG, Park, SK, Cho, HS & Soh, MS 2018, 'A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana', Journal of experimental botany, vol. 69, no. 15, pp. 3609-3623. https://doi.org/10.1093/jxb/ery164

A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana. / Lee, Inhye; Kim, Kuglae; Lee, Sumin; Lee, Seungjun; Hwang, Eunjin; Shin, Kihye; Kim, Dayoung; Choi, Jungki; Choi, Hyunmo; Cha, Jeong Seok; Kim, Hoyoung; Lee, Rin A.; Jeong, Suyeong; Kim, Jeongsik; Kim, Yumi; Nam, Hong Gil; Park, Soon Ki; Cho, Hyun Soo; Soh, Moon Soo.

In: Journal of experimental botany, Vol. 69, No. 15, 27.06.2018, p. 3609-3623.

Research output: Contribution to journalArticle

TY - JOUR

T1 - A missense allele of KARRIKIN-INSENSITIVE2 impairs ligand-binding and downstream signaling in Arabidopsis thaliana

AU - Lee, Inhye

AU - Kim, Kuglae

AU - Lee, Sumin

AU - Lee, Seungjun

AU - Hwang, Eunjin

AU - Shin, Kihye

AU - Kim, Dayoung

AU - Choi, Jungki

AU - Choi, Hyunmo

AU - Cha, Jeong Seok

AU - Kim, Hoyoung

AU - Lee, Rin A.

AU - Jeong, Suyeong

AU - Kim, Jeongsik

AU - Kim, Yumi

AU - Nam, Hong Gil

AU - Park, Soon Ki

AU - Cho, Hyun Soo

AU - Soh, Moon Soo

PY - 2018/6/27

Y1 - 2018/6/27

N2 - A smoke-derived compound, karrikin (KAR), and an endogenous but as yet unidentified KARRIKIN INSENSITIVE2 (KAI2) ligand (KL) have been identified as chemical cues in higher plants that impact on multiple aspects of growth and development. Genetic screening of light-signaling mutants in Arabidopsis thaliana has identified a mutant designated as ply2 (pleiotropic long hypocotyl2) that has pleiotropic light-response defects. In this study, we used positional cloning to identify the molecular lesion of ply2 as a missense mutation of KAI2/HYPOSENSITIVE TO LIGHT, which causes a single amino acid substitution, Ala219Val. Physiological analysis and genetic epistasis analysis with the KL-signaling components MORE AXILLARY GROWTH2 (MAX2) and SUPPRESSOR OF MAX2 1 suggested that the pleiotropic phenotypes of the ply2 mutant can be ascribed to a defect in KL-signaling. Molecular and biochemical analyses revealed that the mutant KAI2 ply2 protein is impaired in its ligand-binding activity. In support of this conclusion, X-ray crystallography studies suggested that the KAI2 ply2 mutation not only results in a narrowed entrance gate for the ligand but also alters the structural flexibility of the helical lid domains. We discuss the structural implications of the Ala219 residue with regard to ligand-specific binding and signaling of KAI2, together with potential functions of KL-signaling in the context of the light-regulatory network in Arabidopsis thaliana.

AB - A smoke-derived compound, karrikin (KAR), and an endogenous but as yet unidentified KARRIKIN INSENSITIVE2 (KAI2) ligand (KL) have been identified as chemical cues in higher plants that impact on multiple aspects of growth and development. Genetic screening of light-signaling mutants in Arabidopsis thaliana has identified a mutant designated as ply2 (pleiotropic long hypocotyl2) that has pleiotropic light-response defects. In this study, we used positional cloning to identify the molecular lesion of ply2 as a missense mutation of KAI2/HYPOSENSITIVE TO LIGHT, which causes a single amino acid substitution, Ala219Val. Physiological analysis and genetic epistasis analysis with the KL-signaling components MORE AXILLARY GROWTH2 (MAX2) and SUPPRESSOR OF MAX2 1 suggested that the pleiotropic phenotypes of the ply2 mutant can be ascribed to a defect in KL-signaling. Molecular and biochemical analyses revealed that the mutant KAI2 ply2 protein is impaired in its ligand-binding activity. In support of this conclusion, X-ray crystallography studies suggested that the KAI2 ply2 mutation not only results in a narrowed entrance gate for the ligand but also alters the structural flexibility of the helical lid domains. We discuss the structural implications of the Ala219 residue with regard to ligand-specific binding and signaling of KAI2, together with potential functions of KL-signaling in the context of the light-regulatory network in Arabidopsis thaliana.

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