In "strategy 1" plants, several alterations in root physiology and morpholo
gy are induced by Fe deficiency, although the mechanisms by which low Fe le
vels are translated into reactions aimed at alleviating Fe shortage are lar
gely unknown. To prove whether changes in hormone concentration or sensitiv
ity are involved in the adaptation to suboptimal Fe availability, we tested
45 mutants of Arabidopsis defective in hormone metabolism and/or root hair
formation for their ability to increase Fe(lll) chelate reductase activity
and to initiate the formation and enlargement of root hairs. Activity stai
ning for ferric chelate reductase revealed that all mutants were responsive
to Fe deficiency, suggesting that hormones are not necessary for the induc
tion. Treatment of wild-type plants with the ethylene precursor 1-aminocycl
opropane-1-carboxylic acid caused the development of root hairs in location
s normally occupied by non-hair cells, but did not stimulate ferric reducta
se activity. Ectopic root hairs were also formed in -Fe roots, suggesting a
role for ethylene in the morphological responses to Fe deficiency. Ultrast
ructural analysis of rhizodermal cells indicated that neither Fe deficiency
nor 1-aminocyclopropane-1-carboxylic acid treatment caused transfer-cell-l
ike alterations in Arabidopsis roots. Our data indicate that the morphologi
cal and physiological components of the Fe stress syndrome are regulated se
parately.