Lotus japonicus SUNERGOS1 encodes a predicted subunit A of a DNA topoisomerase VI and is required for nodule differentiation and accommodation of rhizobial infection

TY - JOUR

T1 - Lotus japonicus SUNERGOS1 encodes a predicted subunit A of a DNA topoisomerase VI and is required for nodule differentiation and accommodation of rhizobial infection

AU - Yoon, Hwi Joong

AU - Hossain, Md Shakhawat

AU - Held, Mark

AU - Hou, Hongwei

AU - Kehl, Marilyn

AU - Tromas, Alexandre

AU - Sato, Shusei

AU - Tabata, Satoshi

AU - Andersen, Stig Uggerhøj

AU - Stougaard, Jens

AU - Ross, Loretta

AU - Szczyglowski, Krzysztof

N1 - This article is protected by copyright. All rights reserved.

PY - 2014/6

Y1 - 2014/6

N2 - A symbiotic mutant of Lotus japonicus, called sunergos1-1 (suner1-1), originated from a har1-1 suppressor screen. suner1-1 supports epidermal infection by Mesorhizobium loti and initiates cell divisions for nodule primordia organogenesis. However, these processes appear to be temporarily stalled early during symbiotic interaction leading to a low nodule number phenotype. This defect is ephemeral and near wild-type nodule numbers are reached by suner1-1 at a later point after infection. Using an approach that combined map-based cloning and next-generation sequencing, we have identified the causative mutation and show that the suner1-1 phenotype is determined by a weak recessive allele, with the corresponding wild-type SUNER1 locus encoding a predicted subunit A of a DNA topoisomerase VI. Our data suggest that at least one function of SUNER1 during symbiosis is to participate in endoreduplication, which is an essential step during normal differentiation of functional, nitrogen-fixing nodules. This article is protected by copyright. All rights reserved.

AB - A symbiotic mutant of Lotus japonicus, called sunergos1-1 (suner1-1), originated from a har1-1 suppressor screen. suner1-1 supports epidermal infection by Mesorhizobium loti and initiates cell divisions for nodule primordia organogenesis. However, these processes appear to be temporarily stalled early during symbiotic interaction leading to a low nodule number phenotype. This defect is ephemeral and near wild-type nodule numbers are reached by suner1-1 at a later point after infection. Using an approach that combined map-based cloning and next-generation sequencing, we have identified the causative mutation and show that the suner1-1 phenotype is determined by a weak recessive allele, with the corresponding wild-type SUNER1 locus encoding a predicted subunit A of a DNA topoisomerase VI. Our data suggest that at least one function of SUNER1 during symbiosis is to participate in endoreduplication, which is an essential step during normal differentiation of functional, nitrogen-fixing nodules. This article is protected by copyright. All rights reserved.

U2 - 10.1111/tpj.12520

DO - 10.1111/tpj.12520

M3 - Journal article

C2 - 24661810

SN - 0960-7412

VL - 78

SP - 811

EP - 821

JO - Plant Journal

JF - Plant Journal

IS - 5

ER -