SummaryA series of mutants of Arabidopsis thaliana 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 pin‐formed mutants and mutations at a new locus named pinoid. As well as causing inflorescence defects, pinoid 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 PINOID controls an early general step in meristem development. pinoid mutant defects are similar to those seen in pin‐formed 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 pin‐formed mutant phenotype, but in young inflorescence stems of even the strongest pinoid 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 pinoid mutants rather than being directly controlled by the PINOID gene product. Even so, double mutant studies indicate that the process controlled by PINOID overlaps with that specified by the AUXIN RESISTANT1 gene, suggesting that PINOID plays some role in an auxin‐related process.

Bennett, S. R. M., Alvarez, J., Bossinger, G., & Smyth, D. R. (1995). Morphogenesis in pinoid mutants of Arabidopsis thaliana. The Plant Journal, 8(4), 505–520. Portico.