Morphogenesis in <i>pinoid</i> mutants of <i>Arabidopsis thaliana</i>

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<jats:title>Summary</jats:title><jats:p>A series of mutants of <jats:italic>Arabidopsis thaliana</jats:italic> was selected in which the inflorescence stem elongates but loses the ability to produce flower primordia on its flanks. Mutants fell into two classes, further occurrences of <jats:italic>pin‐formed</jats:italic> mutants and mutations at a new locus named <jats:italic>pinoid</jats:italic>. As well as causing inflorescence defects, <jats:italic>pinoid</jats:italic> mutations result in pleiotropic defects in the development of floral organs, cotyledons and leaves. Most changes involve the number of organs produced rather than their differentiation suggesting that <jats:italic>PINOID</jats:italic> controls an early general step in meristem development. <jats:italic>pinoid</jats:italic> mutant defects are similar to those seen in <jats:italic>pin‐formed</jats:italic> mutants for inflorescences and flowers, but different for cotyledons and leaves indicating that the two genes have separate but overlapping functions. A defect in polar auxin transport is implicated in the <jats:italic>pin‐formed</jats:italic> mutant phenotype, but in young inflorescence stems of even the strongest <jats:italic>pinoid</jats:italic> mutants it occurs at close to wild‐type levels. It is markedly reduced only after stems have ceased elongating. Thus, it is likely that polar auxin transport is secondarily affected in <jats:italic>pinoid</jats:italic> mutants rather than being directly controlled by the <jats:italic>PINOID</jats:italic> gene product. Even so, double mutant studies indicate that the process controlled by <jats:italic>PINOID</jats:italic> overlaps with that specified by the <jats:italic>AUXIN RESISTANT1</jats:italic> gene, suggesting that <jats:italic>PINOID</jats:italic> plays some role in an auxin‐related process.</jats:p>

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