Mohrholz, A.; Sun, H.; Glöckner, N.; Hummel, S.; Kolukisaoglu, Ü.; Schneeberger, K.; Harter, K. The Striking Flower-in-Flower Phenotype of Arabidopsis thaliana Nossen (No-0) is Caused by a Novel LEAFY Allele. Plants2019, 8, 599.
Mohrholz, A.; Sun, H.; Glöckner, N.; Hummel, S.; Kolukisaoglu, Ü.; Schneeberger, K.; Harter, K. The Striking Flower-in-Flower Phenotype of Arabidopsis thaliana Nossen (No-0) is Caused by a Novel LEAFY Allele. Plants 2019, 8, 599.
Mohrholz, A.; Sun, H.; Glöckner, N.; Hummel, S.; Kolukisaoglu, Ü.; Schneeberger, K.; Harter, K. The Striking Flower-in-Flower Phenotype of Arabidopsis thaliana Nossen (No-0) is Caused by a Novel LEAFY Allele. Plants2019, 8, 599.
Mohrholz, A.; Sun, H.; Glöckner, N.; Hummel, S.; Kolukisaoglu, Ü.; Schneeberger, K.; Harter, K. The Striking Flower-in-Flower Phenotype of Arabidopsis thaliana Nossen (No-0) is Caused by a Novel LEAFY Allele. Plants 2019, 8, 599.
Abstract
The transition to reproduction is a crucial step in the life cycle of any organism. In Arabidopsis thaliana the establishment of reproductive growth can be divided into two phases: Firstly, cauline leaves with axillary meristems are formed and internode elongation begins. Secondly, lateral meristems develop into flowers with defined organs. Floral shoots are usually determinate and suppress the development of lateral shoots. Here, we describe a transposon insertion mutant in the Nossen accession with defects in floral development and growth. Most strikingly is the outgrowth of stems from the axillary bracts of the primary flower carrying secondary flowers. Therefore, we named this mutant flower-in-flower (fif). However, the transposon insertion in the annotated gene is not the cause for the fif phenotype. By means of classical and genome sequencing-based mapping, the mutation responsible for the fif phenotype was found to be in the LEAFY gene. The mutation, a G-to-A exchange in the second exon of LEAFY, creates a novel lfy allele and results in a cysteine-to-tyrosine exchange in the α1-helix of LEAFY´s DNA-binding domain. This exchange abolishes target DNA-binding, whereas subcellular localization and homomerization are not affected. To explain the strong fif phenotype against this molecular findings, several hypotheses are discussed.
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