Structure-function analysis of interallelic complementation inROOTYtransheterozygotes

Abstract

<jats:title>Abstract</jats:title><jats:p>Auxin is a crucial plant growth regulator. Forward genetic screens for auxin-related mutants have led to the identification of key genes involved in auxin biosynthesis, transport, and signaling. Loss-of-function mutations in the genes involved in indole glucosinolate biosynthesis, a metabolically-related route that produces defense compounds from indolic precursors shared with the auxin pathway, result in auxin overproduction. We identified an allelic series of fertile, hypomorphic mutants for an essential indole glucosinolate route gene <jats:italic>ROOTY</jats:italic> (<jats:italic>RTY)</jats:italic> that show a range of high-auxin defects. Genetic characterization of these lines uncovered phenotypic suppression by <jats:italic>cyp79b2 b3</jats:italic>, <jats:italic>wei2</jats:italic>, and <jats:italic>wei7</jats:italic> mutants and revealed the phenomenon of interallelic complementation in several <jats:italic>RTY</jats:italic> transheterozygotes. Structural modeling of RTY shed light on the structure-to-function relations in the RTY homo- and heterodimers and unveiled the likely structural basis of interallelic complementation. This work underscores the importance of employing true null mutants in genetic complementation studies.</jats:p>