A seed-specific transcription factor, HSFA9, anticipates UV-B light responses by mimicking the activation of the UV-B receptor in tobacco.

Sunflower heat shock factor A9 (HSFA9, hereafter A9) is a transcription factor involved in seed desiccation tolerance and longevity. A9 also links the regulation of seed maturation with that of seedling photomorphogenesis through visible light receptors. Analyses in transgenic Nicotiana tabacum (tobacco) indicated that A9 also affects responses mediated by NtUVR8, the receptor of ultraviolet light B (UV-B).

Heat Stress Factors Expressed during Seed Maturation Differentially Regulate Seed Longevity and Seedling Greening.

Heat Stress Factor A9 (A9), a seed-specific transcription factor contributing to seed longevity, also enhances phytochrome-dependent seedling greening. The RNA-seq analyses of imbibed-seed transcripts here reported indicated potential additional effects of A9 on cryptochrome-mediated blue-light responses. These analyses also suggested that in contrast to the A9 effects on longevity, which require coactivation by additional factors as A4a, A9 alone might suffice for the enhancement of photomorphogenesis at the seedling stage.

SUMO-Dependent Synergism Involving Heat Shock Transcription Factors with Functions Linked to Seed Longevity and Desiccation Tolerance.

A transcriptional synergism between HaHSFA9 (A9) and HaHSFA4a (A4a) contributes to determining longevity and desiccation tolerance of sunflower (, L.) seeds. Potential lysine SUMOylation sites were identified in A9 and A4a and mutated to arginine.

Seed-specific transcription factor HSFA9 links late embryogenesis and early photomorphogenesis.

HSFA9 is a seed-specific transcription factor that in sunflower (Helianthus annuus) is involved in desiccation tolerance and longevity. Here we show that the constitutive overexpression of HSFA9 in tobacco (Nicotiana tabacum) seedlings attenuated hypocotyl growth under darkness and accelerated the initial photosynthetic development. Plants overexpressing HSFA9 increased accumulation of carotenoids, chlorophyllide, and chlorophyll, and displayed earlier unfolding of the cotyledons.

Heat shock transcription factors involved in seed desiccation tolerance and longevity retard vegetative senescence in transgenic tobacco.

Transcription factors normally expressed in sunflower seeds delayed vegetative senescence induced by severe stress in transgenic tobacco. This revealed a novel connection between seed heat shock factors, desiccation tolerance and vegetative longevity. HaHSFA9 and HaHSFA4a coactivate a genetic program that, in sunflower (Helianthus annuus L.

Co-overexpression of two Heat Shock Factors results in enhanced seed longevity and in synergistic effects on seedling tolerance to severe dehydration and oxidative stress.

Background: We have previously reported that the seed-specific overexpression of sunflower (Helianthus annuus L.) Heat Shock Factor A9 (HaHSFA9) enhanced seed longevity in transgenic tobacco (Nicotiana tabacum L.).

Protection of the photosynthetic apparatus from extreme dehydration and oxidative stress in seedlings of transgenic tobacco.

A genetic program that in sunflower seeds is activated by Heat Shock transcription Factor A9 (HaHSFA9) has been analyzed in transgenic tobacco seedlings. The ectopic overexpression of the HSFA9 program protected photosynthetic membranes, which resisted extreme dehydration and oxidative stress conditions. In contrast, heat acclimation of seedlings induced thermotolerance but not resistance to the harsh stress conditions employed.

Repression by an auxin/indole acetic acid protein connects auxin signaling with heat shock factor-mediated seed longevity.

The plant hormone auxin regulates growth and development by modulating the stability of auxin/indole acetic acid (Aux/IAA) proteins, which in turn repress auxin response factors (ARFs) transcriptional regulators. In transient assays performed in immature sunflower embryos, we observed that the Aux/IAA protein HaIAA27 represses transcriptional activation by HaHSFA9, a heat shock transcription factor (HSF). We also found that HaIAA27 is stabilized in immature sunflower embryos, where we could show bimolecular fluorescence complementation interaction between native forms of HaIAA27 and HaHSFA9.

Loss of function of the HSFA9 seed longevity program.

Gain of function approaches that have been published by our laboratory determined that HSFA9 (Heat Shock Factor A9) activates a genetic program contributing to seed longevity and to desiccation tolerance in plant embryos. We now evaluate the role(s) of HSFA9 by loss of function using different modified forms of HaHSFA9 (sunflower HSFA9), which were specifically overexpressed in seeds of transgenic tobacco. We used two inactive forms (M1, M2) with deletion or mutation of the transcription activation domain of HaHSFA9, and a third form (M3) with HaHSFA9 converted to a potent active repressor by fusion of the SRDX motif.

The HaDREB2 transcription factor enhances basal thermotolerance and longevity of seeds through functional interaction with HaHSFA9.

Background: Transcription factor HaDREB2 was identified in sunflower (Helianthus annuus L.) as a drought-responsive element-binding factor 2 (DREB2) with unique properties. HaDREB2 and the sunflower Heat Shock Factor A9 (HaHSFA9) co-activated the Hahsp17.

The ectopic overexpression of a seed-specific transcription factor, HaHSFA9, confers tolerance to severe dehydration in vegetative organs.

Most plant seeds tolerate desiccation, but vegetative tissues are intolerant to drastic dehydration, except in the case of resurrection plants. Therefore, changes in the regulation of genes normally expressed in seeds are thought to be responsible for the evolutionary origin of desiccation tolerance in resurrection plants. Here, we show that constitutive overexpression of the seed-specific HSFA9 transcription factor from sunflower is sufficient to confer tolerance to severe dehydration, outside of the developing seed context, to vegetative tissues of transgenic tobacco.

Distinct heat-shock element arrangements that mediate the heat shock, but not the late-embryogenesis induction of small heat-shock proteins, correlate with promoter activation in root-knot nematode feeding cells.

Genes coding small heat-shock proteins (sHSPs) show distinct behaviours with respect to environmental and developmental signals. Their transcriptional regulation depends on particular combinations of heat stress cis-elements (heat-shock elements; HSEs) but many aspects regarding their regulation remain unclear. Cyst and root-knot nematodes induce, in the roots of infected plants, the differentiation of special feeding cells with high metabolic activity (syncytia and giant cells, respectively), a process accompanied by extensive gene expression changes.

Improved resistance to controlled deterioration in transgenic seeds.

We show that seed-specific overexpression of the sunflower (Helianthus annuus) HaHSFA9 heat stress transcription factor (HSF) in tobacco (Nicotiana tabacum) enhances the accumulation of heat shock proteins (HSPs). Among these proteins were HSP101 and a subset of the small HSPs, including proteins that accumulate only during embryogenesis in the absence of thermal stress. Levels of late embryogenesis abundant proteins or seed oligosaccharides, however, were not affected.

Functional interaction between two transcription factors involved in the developmental regulation of a small heat stress protein gene promoter.

Hahsp17.6G1 is the promoter of a small heat stress protein (sHSP) from sunflower (Helianthus annuus) that is activated during zygotic embryogenesis, but which does not respond to heat stress. We report here the cloning of a transcription factor (TF), sunflower drought-responsive element binding factor 2 (HaDREB2), by one-hybrid interaction with functional cis-elements in Hahsp17.

Induction of the Hahsp17.7G4 promoter by root-knot nematodes: involvement of heat-shock elements in promoter activity in giant cells.

Root-knot nematodes feed from specialized giant cells induced in the plants that they parasitize. We found that the promoter of the Hahsp17.7G4 gene, which encodes a small heat-shock protein involved in embryogenesis and stress responses, directed GUS expression in tobacco galls induced by the root-knot nematode Meloidogyne incognita.

A seed-specific heat-shock transcription factor involved in developmental regulation during embryogenesis in sunflower.

We report the cloning and functional characterization of the first heat-shock transcription factor that is specifically expressed during embryogenesis in the absence of environmental stress. In sunflower embryos this factor, HaHSFA9, trans-activated promoters with poor consensus heat-shock cis-elements, including that of the seed-specific Hahsp17.6G1 gene.

Selective activation of the developmentally regulated Ha hsp17.6 G1 promoter by heat stress transcription factors.

Using two well-characterized heat stress transcription factors (Hsfs) from tomato (Lycopersicon peruvianum; LpHsfA1 and LpHsfA2), we analyzed the transcriptional activation of the Ha hsp17.6 G1 promoter in sunflower (Helianthus annuus) embryos. In this system, we observed transient promoter activation only with LpHsfA2.

Reversible heat-induced inactivation of chimeric beta-glucuronidase in transgenic plants.

We compared the expression patterns in transgenic tobacco (Nicotiana tabacum) of two chimeric genes: a translational fusion to beta-glucuronidase (GUS) and a transcriptional fusion, both with the same promoter and 5'-flanking sequences of Ha hsp17.7 G4, a small heat shock protein (sHSP) gene from sunflower (Helianthus annuus). We found that immediately after heat shock, the induced expression from the two fusions in seedlings was similar, considering chimeric mRNA or GUS protein accumulation.