The aim of this work was to clarify the role of S supply in the development of the response to Fe depletion in Strategy I plants. In S-sufficient plants, Fe-deficiency caused an increase in the Fe(III)-chelate reductase activity, (59)Fe uptake rate and ethylene production at root level. This response was associated with increased expression of LeFRO1 [Fe(III)-chelate reductase] and LeIRT1 (Fe(2+) transporter) genes. Instead, when S-deficient plants were transferred to a Fe-free solution, no induction of Fe(III)-chelate reductase activity and ethylene production was observed. The same held true for LeFRO1 gene expression, while the increase in (59)Fe(2+) uptake rate and LeIRT1 gene over-expression were limited. Sulphur deficiency caused a decrease in total sulphur and thiol content; a concomitant increase in (35)SO(4) (2-) uptake rate was observed, this behaviour being particularly evident in Fe-deficient plants. Sulphur deficiency also virtually abolished expression of the nicotianamine synthase gene (LeNAS), independently of the Fe growth conditions. Sulphur deficiency alone also caused a decrease in Fe content in tomato leaves and an increase in root ethylene production; however, these events were not associated with either increased Fe(III)-chelate reductase activity, higher rates of (59)Fe uptake or over-expression of either LeFRO1 or LeIRT1 genes. Results show that S deficiency could limit the capacity of tomato plants to cope with Fe-shortage by preventing the induction of the Fe(III)-chelate reductase and limiting the activity and expression of the Fe(2+) transporter. Furthermore, the results support the idea that ethylene alone cannot trigger specific Fe-deficiency physiological responses in a Strategy I plant, such as tomato.
Sulphur deprivation limits Fe-deficiency responses in tomato plants
VARANINI, Zeno;
2009-01-01
Abstract
The aim of this work was to clarify the role of S supply in the development of the response to Fe depletion in Strategy I plants. In S-sufficient plants, Fe-deficiency caused an increase in the Fe(III)-chelate reductase activity, (59)Fe uptake rate and ethylene production at root level. This response was associated with increased expression of LeFRO1 [Fe(III)-chelate reductase] and LeIRT1 (Fe(2+) transporter) genes. Instead, when S-deficient plants were transferred to a Fe-free solution, no induction of Fe(III)-chelate reductase activity and ethylene production was observed. The same held true for LeFRO1 gene expression, while the increase in (59)Fe(2+) uptake rate and LeIRT1 gene over-expression were limited. Sulphur deficiency caused a decrease in total sulphur and thiol content; a concomitant increase in (35)SO(4) (2-) uptake rate was observed, this behaviour being particularly evident in Fe-deficient plants. Sulphur deficiency also virtually abolished expression of the nicotianamine synthase gene (LeNAS), independently of the Fe growth conditions. Sulphur deficiency alone also caused a decrease in Fe content in tomato leaves and an increase in root ethylene production; however, these events were not associated with either increased Fe(III)-chelate reductase activity, higher rates of (59)Fe uptake or over-expression of either LeFRO1 or LeIRT1 genes. Results show that S deficiency could limit the capacity of tomato plants to cope with Fe-shortage by preventing the induction of the Fe(III)-chelate reductase and limiting the activity and expression of the Fe(2+) transporter. Furthermore, the results support the idea that ethylene alone cannot trigger specific Fe-deficiency physiological responses in a Strategy I plant, such as tomato.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.