UVSSA, UBP12, and RDO2/TFIIS Contribute to Arabidopsis UV Tolerance.

Plant DNA is damaged by exposure to solar radiation, which includes ultraviolet (UV) rays. UV damaged DNA is repaired either by photolyases, using visible light energy, or by nucleotide excision repair (NER), also known as dark repair. NER consists of two subpathways: global genomic repair (GGR), which repairs untranscribed DNA throughout the genome, and transcription-coupled repair (TCR), which repairs transcribed DNA.

RAD7 homologues contribute to Arabidopsis UV tolerance.

Frequent exposure of plants to solar ultraviolet radiation (UV) results in damaged DNA. One mechanism of DNA repair is the light independent pathway Global Genomic Nucleotide Excision Repair (GG-NER), which repairs UV damaged DNA throughout the genome. In mammals, GG-NER DNA damage recognition is performed by the Damaged DNA Binding protein 1 and 2 (DDB1/2) complex which recruits the Xeroderma Pigmentosa group C (XPC) / RAD23D complex.

Role of Arabidopsis ABF1/3/4 during det1 germination in salt and osmotic stress conditions.

Arabidopsis det1 mutants exhibit salt and osmotic stress resistant germination. This phenotype requires HY5, ABF1, ABF3, and ABF4. While DE-ETIOLATED 1 (DET1) is well known as a negative regulator of light development, here we describe how det1 mutants also exhibit altered responses to salt and osmotic stress, specifically salt and mannitol resistant germination.

RAD4 and RAD23/HMR Contribute to Arabidopsis UV Tolerance.

In plants, exposure to solar ultraviolet (UV) light is unavoidable, resulting in DNA damage. Damaged DNA causes mutations, replication arrest, and cell death, thus efficient repair of the damaged DNA is essential. A light-independent DNA repair pathway called nucleotide excision repair (NER) is conserved throughout evolution.

Arabidopsis DDB1-CUL4 E3 ligase complexes in det1 salt/osmotic stress resistant germination.

A key regulatory mechanism in plant growth, development, and stress signaling utilizes E3 ubiquitin ligases, which target a variety of substrates for degradation. DE-ETIOLATED 1 (DET1) forms a complex with DDB1 (DAMAGED DNA BINDING protein 1) and CUL4 (CULLIN 4), and negatively regulates light signaling. Another DDB1-CUL4 complex containing DWA1 and DWA2 (DWD hypersensitive to ABA 1 and 2) has been shown to negatively regulate abscisic acid (ABA) signaling.

Genetic interactions between DET1 and intermediate genes in Arabidopsis ABA signalling.

Seed germination is regulated positively by light and negatively by the dormancy-promoting phytohormone abscisic acid (ABA). DE-ETIOLATED 1 (DET1) is a negative regulator of light signalling in Arabidopsis thaliana. In contrast, the bZIP transcription factor LONG HYPOCOTYL 5 (HY5) is a positive regulator of light signalling.

Light and COP1 regulate level of overexpressed DET1 protein.

de-etiolated 1 (det1) and constitutive photomorphogenic 1 (cop1) were initially identified as constitutively photomorphogenic Arabidopsis mutants, exhibiting light-grown phenotypes in the dark. Subsequently, both were shown to be components of Damaged DNA Binding protein 1 (DDB1)/CULLIN4-type complexes. Arabidopsis has two DDB1 homologues, DDB1A and DDB1B, and DDB1A mutants enhance det1 phenotypes.

GEm-Related 5 (GER5), an ABA and stress-responsive GRAM domain protein regulating seed development and inflorescence architecture.

We have identified an abscisic acid (ABA) and stress-responsive GRAM (Glucosyltransferases, Rab-like GTPase activators and Myotubularins) domain protein GER5 (GEm-Related 5) closely related to GEM (GLABRA2 Expression Modulator), a novel regulator of cell division and cell fate determination in epidermal cells. A loss-of-function T-DNA line (ger5-2) and transgenic lines silencing (GER5(RNAi)) or overexpressing (GER5(OE)) GER5 displayed several defects in reproductive development affecting seed and embryo development. RNA in situ studies revealed GER5 and related GRAM genes (GEM and GEm-Related 1 (GER1)) have both overlapping and unique expression domains in male and female reproductive organs.

Interactions between Arabidopsis DNA repair genes UVH6, DDB1A, and DDB2 during abiotic stress tolerance and floral development.

Plants must protect themselves from a spectrum of abiotic stresses. For example, the sun is a source of heat, intense light, and DNA-damaging ultraviolet (UV) rays. Damaged DNA binding protein 1A (DDB1A), DDB2, and UV hypersensitive 6 (UVH6)/XPD are all involved in the repair of UV-damaged DNA - DDB1A and DDB2 in the initial damage recognition stage, while the UVH6/XPD helicase unwinds the damaged strand.

Genetic interactions between Arabidopsis DET1 and UVH6 during development and abiotic stress response.

Plants must adapt to a variety of abiotic inputs, including visible light, ultraviolet (UV) light, and heat. In Arabidopsis thaliana, DE-ETIOLATED 1 (DET1) plays a role in visible light signaling, UV tolerance, and development. UV-HYPERSENSITIVE 6 (UVH6) mutants are UV and heat sensitive, as well as dwarf and pale, like det1.

Transcriptional response of abscisic acid (ABA) metabolism and transport to cold and heat stress applied at the reproductive stage of development in Arabidopsis thaliana.

The phytohormone abscisic acid (ABA) plays an important role in developmental processes in addition to mediating plant adaptation to stress. In the current study, transcriptional response of 17 genes involved in ABA metabolism and transport has been examined in vegetative and reproductive organs exposed to cold and heat stress. Temperature stress activated numerous genes involved in ABA biosynthesis, catabolism and transport; however, several ABA biosynthesis genes (ABA1, ABA2, ABA4, AAO3, NCED3) were differentially expressed (up- or down-regulated) in an organ-specific manner.

Effect of overexpression of Arabidopsis damaged DNA-binding protein 1A on de-etiolated 1.

In Arabidopsis thaliana, de-etiolated 1 mutants (det1) grown in the dark resemble light-grown wild-type seedlings. Arabidopsis DET1 encodes a 62 kD protein, which is a negative regulator of light signaling. UV-damaged DNA-binding protein 1 (DDB1) was initially identified due to its role in human DNA damage repair.

Overexpression of Arabidopsis damaged DNA binding protein 1A (DDB1A) enhances UV tolerance.

Damaged DNA Binding protein 1 (DDB1) is a conserved protein and a component of multiple cellular complexes. Arabidopsis has two homologues of DDB1: DDB1A and DDB1B. In this study we examine the role of DDB1A in Arabidopsis UV tolerance and DNA repair using a DDB1A null mutant (ddb1a) and overexpression lines.

DDB2, DDB1A and DET1 exhibit complex interactions during Arabidopsis development.

Damaged DNA-binding proteins 1 and 2 (DDB1 and DDB2) are subunits of the damaged DNA-binding protein complex (DDB). DDB1 is also found in the same complex as DE-ETIOLATED 1 (DET1), a negative regulator of light-mediated responses in plants. Arabidopsis has two DDB1 homologs, DDB1A and DDB1B.

Color of illumination during growth affects LHCII chiral macroaggregates in pea plant leaves.

To determine whether the color of illumination under which plants are grown, affects the structure of photosynthetic antennae, pea plants were grown under either blue-enriched, red-enriched, or white light. Carotenoid content of isolated chloroplasts was found to be insensitive to the color of illumination during growth, while chlorophyll a/b ratio in chloroplasts isolated from young illuminated leaves showed susceptibility to color. Color of illumination affects the LHCII chiral macroaggregates in intact leaves and isolated chloroplasts, providing light-induced alteration of the handedness of the LHCII chiral macroaggregate, as measured with circular dichroism and circularly polarized luminescence.

De-etiolated 1 and damaged DNA binding protein 1 interact to regulate Arabidopsis photomorphogenesis.

Background: Plant development is exquisitely sensitive to light. Seedlings grown in the dark have a developmentally arrested etiolated phenotype, whereas in the light they develop leaves and complete their life cycle. Arabidopsis de-etiolated 1 (det1) mutants develop like light-grown seedlings even when grown in the dark.