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Brassicaceae INDEHISCENT genes specify valve margin cell fate and repress replum formation
Author(s) -
Girin Thomas,
Stephenson Pauline,
Goldsack Cassandra M. P.,
Kempin Sherry A.,
Perez Amandine,
Pires Nuno,
Sparrow Penelope A.,
Wood Thomas A.,
Yanofsky Martin F.,
Østergaard Lars
Publication year - 2010
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2010.04244.x
Subject(s) - arabidopsis , brassicaceae , silique , arabidopsis thaliana , biology , mutant , gene , genetics , botany , microbiology and biotechnology
Summary Members of the Brassicaceae family, including Arabidopsis thaliana and oilseed rape ( Brassica napus ), produce dry fruits that open upon maturity along a specialised tissue called the valve margin. Proper development of the valve margin in Arabidopsis is dependent on the INDEHISCENT ( IND ) gene, the role of which in genetic and hormonal regulation has been thoroughly characterised. Here we perform phylogenetic comparison of IND genes in Arabidopsis and Brassica to identify conserved regulatory sequences that are responsible for specific expression at the valve margin. In addition we have taken a comparative development approach to demonstrate that the BraA.IND.a and BolC.IND.a genes from B. rapa and B. oleracea share identical function with Arabidopsis IND since ethyl methanesulphonate (EMS) mutant alleles and silenced transgenic lines have valve margin defects. Furthermore we show that the degree of these defects can be fine‐tuned for crop improvement. Wild‐type Arabidopsis produces an outer replum composed of about six cell files at the medial region of the fruits, whereas Brassica fruits lack this tissue. A strong loss‐of‐function braA.ind.a mutant gained outer replum tissue in addition to its defect in valve margin development. An enlargement of replum size was also observed in the Arabidopsis ind mutant suggesting a general role of Brassicaceae IND genes in preventing valve margin cells from adopting replum identity.