Microbial Adaptation to Aluminum

Abstract

The presence of aluminum in a minimal mineral medium, with citrate as the sole source of carbon, elicited the production of an exocellular lipid‐rich residue in Pseudomonas fluorescens. Although aluminum affected the growth rate, no apparent diminution in cellular yield was observed in medium supplemented with up to 3 mM of the trivalent metal. While a 10% reduction in cellular yield was recorded in medium with 7.5 mM aluminum, a decrease of 69% was reported in medium supplemented with 50 mM aluminum at stationary phase of growth. The wet weight of the pellet ranged from 5.9 to 70.3 mg mL−1 of culture in medium supplemented with 1–30 mM aluminum. The trivalent metal was immobilized in this precipitate and associated with phosphate moieties. Both neutral lipids and phospholipids constituted the pellet. More than 90% of the weight of the wet pellet was lost following lyophilization. The percentage of aluminum immobilized increased with the concentration of trivalent metal in the medium. Preconditioned cells showed an improved growth rate, and the cellular yield was slightly higher than for unadapted cells.

Aluminum Triggers Decreased Aconitase Activity via Fe-S Cluster Disruption and the Overexpression of Isocitrate Dehydrogenase and Isocitrate Lyase

“…Thus, it is not unlikely that other effectors may be recruited to assure the survivability of the microbe in this aluminum citrate environment. The physiological profile of the microbe in aluminum medium clearly points to the participation of other enzymes in this process (33). Indeed, the two enzymes ICL and IDH-NADP ϩ that cleave isocitrate, the product of the isomerization of citrate by Acn, appear to be an integral part of the biochemical strategy invoked by P. fluorescens to survive this toxic challenge.…”

Influence of nutrient solution on Al-tolerance ofPseudomonassp.

“…This complexing ability of phosphorus is taken into account from most authors who use P‐additions not exceeding 10 μmol l −1 nutrient solution [10, 17, 18]. Nevertheless some studies dealing with Al‐toxicity use appreciable amounts of phosphorus in their nutrient solutions (up to 65 mM) [19, 20]. These differences between media are probably the most important reason for the often extremely contradictory results regarding the extent of Al‐tolerance of microorganisms [10, 11].…”

“…These differences between media are probably the most important reason for the often extremely contradictory results regarding the extent of Al‐tolerance of microorganisms [10, 11]. Thus, reports of extremely Al‐tolerant (up to 100 mM Al) microorganisms [19, 20] must be reconsidered critically as Al‐addition is often approximately compensated by equimolar amounts of soluble P‐salts. As is shown in Fig.…”

Subsurface interactions of actinide species and microorganisms: Implications for the bioremediation of actinide-organic mixtures

“…176 Often, extracellular secretions by bacteria are formed in direct response to the presence of toxic metals in solution. 189,[197][198][199] As we will discuss in detail in the following Section, chemical toxicity due to metals is correlated with the aqueous concentration of the free metal ion. Secretion of extracellular complexing agents reduces the free ion concentration by isolating the toxic metal in a non-bioavailable form, either retained in solution as a mobile metal ligand complex or immobilized in a polymeric "slime" layer outside the cell wall.…”

“…Secretion of extracellular complexing agents reduces the free ion concentration by isolating the toxic metal in a non-bioavailable form, either retained in solution as a mobile metal ligand complex or immobilized in a polymeric "slime" layer outside the cell wall. 189,197,198 Direct evidence for extracellular actinide complexation was described by ROBINSON et al, 2~176 who investigated the effect of "microbial metabolites" produced by soil microorganisms on Pu speciation. Depending on the microbial isolate tested, Pu mobility was either enhanced or retarded as compared to the mobility of the Pu-DTPA (diethylenediaminetetraacetic acid) complex.…”