INVESTIGADORES
CHAN Raquel Lia
artículos
Título:
HAHB4, a sunflower HD-Zip protein, integrates signals from the jasmonic acid and ethylene pathways during wounding and biotic stress responses.
Autor/es:
MANAVELLA PABLO ANDRÉS; DEZAR CARLOS ALBERTO; BONAVENTURE GUSTAVO; BALDWIN IAN THOMAS; CHAN RAQUEL LÍA
Revista:
PLANT JOURNAL
Editorial:
WILEY-BLACKWELL PUBLISHING, INC
Referencias:
Año: 2008 vol. 56 p. 376 - 388
ISSN:
0960-7412
Resumen:
The Helianthus annuus (sunflower) HAHB4 transcription factor belongs to the HD-Zip family and its transcript levels are strongly induced when sunflower plants are attacked by herbivores, mechanically damaged or treated with methyl-jasmonic acid (MeJA) or ethylene (ET). Promoter fusion analysis, in Arabidopsis and in sunflower, demonstrated that induction of HAHB4 expression by these treatments is regulated at the transcriptional level. In transiently transformed sunflower plants HAHB4 expression up-regulates the transcript levels of several genes involved in JA biosynthesis and defense-related processes such as production of green leaf volatiles and trypsin protease inhibitors (TPI). In HAHB4 sunflower over-expressing tissue, increased activities of lipoxygenase, hydroperoxide lyase and TPI are detected whereas in HAHB4-silenced tissue these activities are reduced. Transgenic Arabidopsis thaliana and Zea mays plants ecotopically expressing HAHB4 also exhibit higher transcript levels of defense-related genes and when Spodoptera littoralis or Spodoptera frugiperda larvae are placed on each species respectively, larvae consumed less and gain less mass compared to larvae feeding on control plants. Arabidopsis plants ectopically expressing HAHB4 had higher amounts of JA, JA-isoleucine and ET compared to control plants both, before and after wounding, but reduced levels of salicylic acid (SA) after wounding and bacterial infection. We conclude that HAHB4 coordinates phytohormone production during biotic stress responses and mechanical damage, specifically by positively regulating JA and ET production and negatively regulating ET sensitivity and SA accumulation.