recessive antimorphic alleles overcome functionally redundant loci to reveal tso1 function in arabidopsis flowers and meristems隐性antimorphic等位基因克服功能冗余基因座揭示tso1函数拟南芥花和分生组织.pdfVIP
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recessive antimorphic alleles overcome functionally redundant loci to reveal tso1 function in arabidopsis flowers and meristems隐性antimorphic等位基因克服功能冗余基因座揭示tso1函数拟南芥花和分生组织
Recessive Antimorphic Alleles Overcome Functionally
Redundant Loci to Reveal TSO1 Function in Arabidopsis
Flowers and Meristems
1 1,2 1
Paja Sijacic , Wanpeng Wang , Zhongchi Liu *
1 Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland, United States of America, 2 Plant Science Graduate Program,
Department of Plant Science and Landscape Architecture, University of Maryland, College Park, Maryland, United States of America
Abstract
Arabidopsis TSO1 encodes a protein with conserved CXC domains known to bind DNA and is homologous to animal
proteins that function in chromatin complexes. tso1 mutants fall into two classes due to their distinct phenotypes. Class I,
represented by two different missense mutations in the CXC domain, leads to failure in floral organ development, sterility,
and fasciated inflorescence meristems. Class II, represented by a nonsense mutation and a T-DNA insertion line, develops
wild-type–like flowers and inflorescences but shows severely reduced fertility. The phenotypic variability of tso1 alleles
presents challenges in determining the true function of TSO1. In this study, we use artificial microRNA, double mutant
analysis, and bimolecular fluorescence complementation assay to investigate the molecular basis underlying these two
distinct classes of phenotypes. We show that the class I mutants could be converted into class II by artificial microRNA
knockdown of the tso1 mutant transcript, suggesting that class I alleles produce antimorphic mutant proteins that interfere
with functionally redundant loci. We identified one such redundant factor coded by the closely related TSO1 homolog SOL2.
We show that the class I phenotype can be
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