Transcriptional Analysis of Distant Signaling Induced by Insect Elicitors and Mechanical Wounding in Zea mays

When plants are under insect herbivore attack defensive measures are activated not only locally, but also in distant and systemic tissues. While insect elicitors (IE) abundant in the oral secretions of the attacking herbivore are essential in the regulation of induced defenses, little is known about their effects on systemic defense signaling in maize (Zea mays). The goal of this study was therefore to identify genetic markers that can be used to further characterize local and systemic signaling events induced by IE or mechanical wounding (MW). We selected genes for this study based on their putative involvement in signaling (allene oxide synthase), regulation of gene expression (transcription factor MYC7), and in direct defenses (ribosome inactivating protein) and analyzed their expression in different sections of the treated leaf as well as in systemic parts of the same plant. We found the most significant transcript accumulation of the selected genes after treatment with insect elicitors in those parts with increased JA levels. Additionally, treatment with IE did also induce the accumulation of MYC7 transcripts in basal parts of the treated leaf and systemically. MW, in contrast, did induce RIP and AOS only locally, but not MYC7. This local suppression of MYC7 was further studied by adding glutathione (GSH) as an electron donor to MW plants to quench putative α, β-unsaturated carbonyls, which build up to significant levels around the damage site. Indeed, GSH-treated MW plants accumulated MYC7 at the damage site and also produced more volatiles, suggesting a putative redox-regulatory element being involved in the suppression of MYC7. The results presented herein provide evidence for the specific induction of distant signaling events triggered by IE, most likely through electric signaling. Additionally, a putative role for MW-induced α, β-unsaturated carbonyls in the transcriptional regulation of defense genes was discovered

Nitrate deposition in northern hardwood forests and the nitrogen metabolism of Acer saccharum marsh

It is generally assumed that plant assimilation constitutes the major sink for anthropogenic Nitrate NO 3 − deposited in temperate forests because plant growth is usually limited by nitrogen (N) availability. Nevertheless, plants are known to vary widely in their capacity for NO 3 − uptake and assimilation, and few studies have directly measured these parameters for overstory trees. Using a combination of field and greenhouse experiments, we studied the N nutrition of Acer saccharum Marsh. in four northern hardwood forests receiving experimental NO 3 − additions equivalent to 30 kg N ha −1 year −1 . We measured leaf and fine-root nitrate reductase activity (NRA) of overstory trees using an in vivo assay and used 15 N to determine the kinetic parameters of NO 3 − uptake by excised fine roots. In two greenhouse experiments, we measured leaf and root NRA in A. saccharum seedlings fertilized with 0–3.5 g NO 3 − −N m −2 and determined the kinetic parameters of NO 3 − and NH 4 + uptake in excised roots of seedlings. In both overstory trees and seedlings, rates of leaf and fine root NRA were substantially lower than previously reported rates for most woody plants and showed no response to NO 3 − fertilization (range = non-detectable to 33 nmol NO 2 − g −1 h −1 ). Maximal rates of NO 3 − uptake in overstory trees also were low, ranging from 0.2 to 1.0 μmol g −1 h −1 . In seedlings, the mean V max for NO 3 − uptake in fine roots (1 μmol g −1 h −1 ) was approximately 30 times lower than the V max for NH 4 + uptake (33 μmol g −1 h −1 ). Our results suggest that A. saccharum satisfies its N demand through rapid NH 4 + uptake and may have a limited capacity to serve as a direct sink for atmospheric additions of NO 3 − .Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47695/1/442_2004_Article_BF00334659.pd

Genetic variation in PARL influences mitochondrian content

Given their involvement in processes necessary for life, mitochondrial damage and subsequent dysfunction can lead to a wide range of human diseases. Previous studies of both animal models and humans have suggested that presenilins-associated rhomboid-like protein (PARL) is a key regulator of mitochondrial integrity and function, and plays a role in cellular apoptosis. As a surrogate measure of mitochondrial integrity, we previously measured mitochondrial content in a Caucasian population consisting of large extended pedigrees, with results highlighting a substantial genetic component to this trait. To assess the inXuence of variation in the PARL gene on mitochondrial content, we re-sequenced 6.5 kb of the gene, identifying 16 SNPs and genotyped these in 1,086 Caucasian individuals, distributed across 170 families. Statistical genetic analysis revealed that one promoter variant, T-191C, exhibited signiWcant eVects (after correction for multiple testing) on mitochondrial content levels. Comparison of the transcription factor binding characteristics of the T-191C promoter SNP by EMSA indicates preferential binding of nuclear factors to the T allele, suggesting functional variation in PARL expression. These results suggest that genetic variation within PARL inXuences mitochondrial abundance and integrity.<br /