Microbial communities play a pivotal role in the functioning of plants by influencing their physiology and development. While many members of the rhizosphere microbiome are beneficial to plant growth, also plant pathogenic microorganisms colonize the rhizosphere striving to break through the protective microbial shield and to overcome the innate plant defense mechanisms in order to cause disease. A third group of microorganisms that can be found in the rhizosphere are the true and opportunistic human pathogenic bacteria, which can be carried on or in plant tissue and may cause disease when introduced into debilitated humans. Although the importance of the rhizosphere microbiome for plant growth has been widely recognized, for the vast majority of rhizosphere microorganisms no knowledge exists. To enhance plant growth and health, it is essential to know which microorganism is present in the rhizosphere microbiome and what they are doing. Here, we review the main functions of rhizosphere microorganisms and how they impact on health and disease. We discuss the mechanisms involved in the multitrophic interactions and chemical dialogues that occur in the rhizosphere. Finally, we highlight several strategies to redirect or reshape the rhizosphere microbiome in favor of microorganisms that are beneficial to plant growth and health.

The rhizosphere microbiome: significance of plant beneficial, plant pathogenic, and human pathogenic microorganisms

Acid soils significantly limit crop production worldwide because approximately 50% of the world's potentially arable soils are acidic. Because acid soils are such an important constraint to agriculture, understanding the mechanisms and genes conferring tolerance to acid soil stress has been a focus of intense research interest over the past decade. The primary limitations on acid soils are toxic levels of aluminum (Al) and manganese (Mn), as well as suboptimal levels of phosphorous (P). This review examines our current understanding of the physiological, genetic, and molecular basis for crop Al tolerance, as well as reviews the emerging area of P efficiency, which involves the genetically based ability of some crop genotypes to tolerate P deficiency stress on acid soils. These are interesting times for this field because researchers are on the verge of identifying some of the genes that confer Al tolerance in crop plants; these discoveries will open up new avenues of molecular/physiological inquiry that should greatly advance our understanding of these tolerance mechanisms. Additionally, these breakthroughs will provide new molecular resources for improving crop Al tolerance via both molecular-assisted breeding and biotechnology.

How do crop plants tolerate acid soils? Mechanisms of aluminum tolerance and phosphorous efficiency.

The rhizosphere is the zone of soil immediately surrounding plant roots that is modified by root activity In this critical zone, plants perceive and respond to their environment As a consequence of normal growth and development, a large range of organic and inorganic substances are exchanged between the root and soil, which inevitably leads to changes in the biochemical and physical properties of the rhizosphere Plants also modify their rhizosphere in response to certain environmental signals and stresses Organic anions are commonly detected in this region, and their exudation from plant roots has now been associated with nutrient deficiencies and inorganic ion stresses This review summarizes recent developments in the understanding of the function, mechanism, and regulation of organic anion exudation from roots The benefits that plants derive from the presence of organic anions in the rhizosphere are described and the potential for biotechnology to increase organic anion exudation is highlighted

Function and mechanism of organic anion exudation from plant roots

Aluminum (Al) is the most abundant metal in the earth's crust, comprising about 7% of its mass. Since many plant species are sensitive to micromolar concentrations of Al, the potential for soils to be Al toxic is considerable. Fortunately, most of the Al is bound by ligands or occurs in other nonphytotoxic forms such as aluminosilicates and precipitates. However, solubilization of this Al is enhanced by low pH and Al toxicity is a major factor limiting plant production on acid soils. Soil acidification can develop naturally when basic cations are leached from soils, but it can be accelerated by some farming practices and by acid rain (Kennedy, 1986). Strategies to maintain production on these soils include the application of lime to raise the soil pH and the use of plants that are tolerant of acid soils. Although Al toxicity has been identified as a problem of acid soils for over 70 years, our knowledge about the primary sites of toxicity and the chain of events that finally affects plant growth remains largely speculative. In this paper we review recent progress that has been made in our understanding of Al toxicity and the mechanisms of Al tolerance in plants.

Aluminum Toxicity and Tolerance in Plants

As sessile organisms, plants have evolved mechanisms that allow them to adapt and survive periods of drought stress. One of the inevitable consequences of drought stress is enhanced ROS production in the different cellular compartments, namely in the chloroplasts, the peroxisomes and the mitochondria. This enhanced ROS production is however kept under tight control by a versatile and cooperative antioxidant system that modulates intracellular ROS concentration and sets the redox-status of the cell. Furthermore, ROS enhancement under stress functions as an alarm signal that triggers acclimatory/defense responses by specific signal transduction pathways that involve H(2)O(2) as secondary messenger. ROS signaling is linked to ABA, Ca(2+) fluxes and sugar sensing and is likely to be involved both upstream and downstream of the ABA-dependent signaling pathways under drought stress. Nevertheless, if drought stress is prolonged over to a certain extent, ROS production will overwhelm the scavenging action of the anti-oxidant system resulting in extensive cellular damage and death.

https://www.tandfonline.com/doi/pdf/10.4161/psb.3.3.5536

Drought stress and reactive oxygen species: Production, scavenging and signaling.

We investigated the role that manganese superoxide dismutase (MnSOD, EC 1·15·1·1), an important enzyme of the antioxidant pathway, may play in aluminium (Al) toxicity/ resistance. A wheat ( Triticum aestivum ) cDNA ( WMnSOD ) was cloned and up-regulation of the transcript was observed in root tips after 24 h exposure to 100 µ µ M Al. The WMnSOD1 under the control of the CaMV 35S promoter was expressed in canola ( Brassica napus ). Transgenic plants were phenotypically normal. Northern analyses showed enhanced levels of the WMnSOD1 and WMnSOD1-GUS transcripts and total SOD activity was 1·5- to 2·5-fold greater in transgenic plants than in wild type (WT) plants. Transgenic (T 1 ) leaf discs showed increased retention of chlorophyll and reduced electrolyte leakage when exposed to methyl viologen (MV) as compared with WT leaf discs, suggesting that transgenic plants were more resistant to oxidative stress. When WT canola plants were exposed to aluminium (0‐200 µ µ µ M ), inhibition of root growth, higher SOD activity and increased levels of malondialdehyde (MDA, an indicator of lipid peroxidation) were observed in roots. Aluminium-induced inhibition of root growth and accumulation of MDA was lower in homozygous transgenic plants (T 2 ) compared with WT plants. Transgenic lines also showed lower synthesis of 1,3- β glucans (callose, a sensitive marker for Al injury) as compared with WT. These data suggest that resistance to Al toxicity can be improved by overexpressing WMnSOD1 .

/pdf/transgenic-brassica-napus-plants-overexpressing-aluminium-1euqsesym3.pdf

Transgenic Brassica napus plants overexpressing aluminium-induced mitochondrial manganese superoxide dismutase cDNA are resistant to aluminium

Aluminum (Al) toxicity is a major constraint for crop production in acid soils, although crop cultivars vary in their tolerance to Al We have investigated the potential role of citrate in mediating Al tolerance in Al-sensitive yeast ( Saccharomyces cerevisiae ; MMYO11) and canola ( Brassica napus cv Westar) Yeast disruption mutants defective in genes encoding tricarboxylic acid cycle enzymes, both upstream (citrate synthase [CS]) and downstream (aconitase [ ACO ] and isocitrate dehydrogenase [ IDH ]) of citrate, showed altered levels of Al tolerance A triple mutant of CS (Δ cit123 ) showed lower levels of citrate accumulation and reduced Al tolerance, whereas Δ aco1 - and Δ idh12 -deficient mutants showed higher accumulation of citrate and increased levels of Al tolerance Overexpression of a mitochondrial CS ( CIT1 ) in MMYO11 resulted in a 2- to 3-fold increase in citrate levels, and the transformants showed enhanced Al tolerance A gene for Arabidopsis mitochondrial CS was overexpressed in canola using an Agrobacterium tumefaciens -mediated system Increased levels of CS gene expression and enhanced CS activity were observed in transgenic lines compared with the wild type Root growth experiments revealed that transgenic lines have enhanced levels of Al tolerance The transgenic lines showed enhanced levels of cellular shoot citrate and a 2-fold increase in citrate exudation when exposed to 150 μm Al Our work with yeast and transgenic canola clearly suggest that modulation of different enzymes involved in citrate synthesis and turnover (malate dehydrogenase, CS, ACO , and IDH ) could be considered as potential targets of gene manipulation to understand the role of citrate metabolism in mediating Al tolerance

/pdf/modulation-of-citrate-metabolism-alters-aluminum-tolerance-33r5wjop6b.pdf

Modulation of Citrate Metabolism Alters Aluminum Tolerance in Yeast and Transgenic Canola Overexpressing a Mitochondrial Citrate Synthase

One of the goals of livestock genomics research is to identify the genetic differences responsible for variation in phenotypic traits, particularly those of economic importance. Characterizing the genetic variation in livestock species is an important step towards linking genes or genomic regions with phenotypes. The completion of the bovine genome sequence and recent advances in DNA sequencing technology allow for in-depth characterization of the genetic variations present in cattle. Here we describe the whole-genome resequencing of two Bos taurus bulls from distinct breeds for the purpose of identifying and annotating novel forms of genetic variation in cattle. The genomes of a Black Angus bull and a Holstein bull were sequenced to 22-fold and 19-fold coverage, respectively, using the ABI SOLiD system. Comparisons of the sequences with the Btau4.0 reference assembly yielded 7 million single nucleotide polymorphisms (SNPs), 24% of which were identified in both animals. Of the total SNPs found in Holstein, Black Angus, and in both animals, 81%, 81%, and 75% respectively are novel. In-depth annotations of the data identified more than 16 thousand distinct non-synonymous SNPs (85% novel) between the two datasets. Alignments between the SNP-altered proteins and orthologues from numerous species indicate that many of the SNPs alter well-conserved amino acids. Several SNPs predicted to create or remove stop codons were also found. A comparison between the sequencing SNPs and genotyping results from the BovineHD high-density genotyping chip indicates a detection rate of 91% for homozygous SNPs and 81% for heterozygous SNPs. The false positive rate is estimated to be about 2% for both the Black Angus and Holstein SNP sets, based on follow-up genotyping of 422 and 427 SNPs, respectively. Comparisons of read depth between the two bulls along the reference assembly identified 790 putative copy-number variations (CNVs). Ten randomly selected CNVs, five genic and five non-genic, were successfully validated using quantitative real-time PCR. The CNVs are enriched for immune system genes and include genes that may contribute to lactation capacity. The majority of the CNVs (69%) were detected as regions with higher abundance in the Holstein bull. Substantial genetic differences exist between the Black Angus and Holstein animals sequenced in this work and the Hereford reference sequence, and some of this variation is predicted to affect evolutionarily conserved amino acids or gene copy number. The deeply annotated SNPs and CNVs identified in this resequencing study can serve as useful genetic tools, and as candidates in searches for phenotype-altering DNA differences.

/pdf/whole-genome-resequencing-of-black-angus-and-holstein-cattle-2vvw9f5iqv.pdf

Whole genome resequencing of black Angus and Holstein cattle for SNP and CNV discovery.

Aluminum Resistance in Triticum aestivum Associated with Enhanced Exudation of Malate

Human studies of the influence of aging and other factors on intermuscular fat (INTMF) were reviewed. Intermuscular fat increased with weight loss, weight gain, or with no weight change with age in humans. An increase in INTMF represents a similar threat to type 2 diabetes and insulin resistance as does visceral adipose tissue (VAT). Studies of INTMF in animals covered topics such as quantitative deposition and genetic relationships with other fat depots. The relationship between leanness and higher proportions of INTMF fat in pigs was not observed in human studies and was not corroborated by other pig studies. In humans, changes in muscle mass, strength and quality are associated with INTMF accretion with aging. Gene expression profiling and intrinsic methylation differences in pigs demonstrated that INTMF and VAT are primarily associated with inflammatory and immune processes. It seems that in the pig and humans, INTMF and VAT share a similar pattern of distribution and a similar association of components dictating insulin sensitivity. Studies on intramuscular (IM) adipocyte development in meat animals were reviewed. Gene expression analysis and genetic analysis have identified candidate genes involved in IM adipocyte development. Intramuscular (IM) adipocyte development in human muscle is only seen during aging and some pathological circumstance. Several genetic links between human and meat animal adipogenesis have been identified. In pigs, the Lipin1 and Lipin 2 gene have strong genetic effects on IM accumulation. Lipin1 deficiency results in immature adipocyte development in human lipodystrophy. In humans, overexpression of Perilipin 2 (PLIN2) facilitates intramyocellular lipid accretion whereas in pigs PLIN2 gene expression is associated with IM deposition. Lipins and perilipins may influence intramuscular lipid regardless of species.

https://www.tandfonline.com/doi/pdf/10.4161/adip.28546

Urmila Basu

Papers

Transgenic Brassica napus plants overexpressing aluminium-induced mitochondrial manganese superoxide dismutase cDNA are resistant to aluminium

Modulation of Citrate Metabolism Alters Aluminum Tolerance in Yeast and Transgenic Canola Overexpressing a Mitochondrial Citrate Synthase

Whole genome resequencing of black Angus and Holstein cattle for SNP and CNV discovery.

Aluminum Resistance in Triticum aestivum Associated with Enhanced Exudation of Malate

Intermuscular and intramuscular adipose tissues: Bad vs. good adipose tissues.