A series of mutants of Arabidopsis thaliana was selected in which the
inflorescence stem elongates but loses the ability to produce flower p
rimordia on its flanks. Mutants fell into two classes, further occurre
nces of pin-formed mutants and mutations at a new locus named pinoid.
As well as causing inflorescence defects, pinoid mutations result in p
leiotropic defects in the development of floral organs, cotyledons and
leaves. Most changes involve the number of organs produced rather tha
n their differentiation suggesting that PINOID controls an early gener
al step in meristem development. pinoid mutant defects are similar to
those seen in pin-formed mutants for inflorescences and flowers, but d
ifferent 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 inflore
scence stems of even the strongest pinoid mutants it occurs at close t
o wild-type levels. It is markedly reduced only after stems have cease
d elongating. Thus, it is likely that polar auxin transport is seconda
rily affected in pinoid mutants rather than being directly controlled
by the PINOID gene product. Even so, double mutant studies indicate th
at the process controlled by PINOID overlaps with that specified by th
e AUXIN RESISTANT1 gene, suggesting that PINOID plays some role in an
auxin-related process.