Cell wall acidification

Auxins modulate root and shoot formation by stimulating extension growth and cell division in the cambium. Cell wall acidification in response to auxins (probably due to stimulation of the plasma membrane H ATPase) at least partly accounts for the loosening of cell walls and stimulation of elongation growth. Auxins also cause membrane hyperpolarization. 

Figure 3. Diagram of a section through the cell wall of Acidithiobacillus ferrooxidans modified from Blake et al. (1992) showing the relationship between iron oxidation and pyrite dissolution. OM =outer membrane, P = periplasm, IM = inner or (cytoplasmic) membrane, cty = cytochrome, pmf = proton motive force. Passage of a proton (driven by proton motive force) into the cell catalyzes the conversion of ADP to ATP. Ferrous iron binds to a component of the electron transport chain, probably a cytochrome c, and is oxidized. The electrons are passed to a terminal reductase where they are combined with O2 and to form water, preventing acidification of the cytoplasm. Ferric iron can either oxidize pyrite (e.g. within the ore body) or form nanocrystalline iron oxyhydroxide minerals (often in surrounding groundwater or streams).

Acidification of urine is affected in renal tubular acidosis. This condition may be due to an inborn error of metabolism or to an acquired tubular lesion. The defect may be related either to the secretion of hydrogen ions or to the diffusion of hydrogen ions into the blood as a result of increased permeability of the distal tubule cell wall to secreted hydrogen ions. Because renal tubular acidosis is primarily a defect in hydrogen ion secretion, the formation of ammonia by tubule cells is not affected. 

Within 10 minutes after lAA application, rapid response mechanisms result in coleoptile and stem segment cell wall deformation and elongation (13). Changes in cell metabolism appear to occur which result in the rapid pumping of protons across the cell plasma membrane and a resulting acidification of the cell wall. This acidification leads by an unknown mechanism to the hydrolysis of noncovalent crosslinks between xyloglucan polymers and the cellulose microfibrils of the cell wall. The cross links are later reformed in the enlarged cell (14). 

This acid growth hypothesis is supported by empirical data including the fact that acid solutions can cause cell elongation mimicking the effects of auxin, and neutral buffers will inhibit the effect of auxin on cell elongation by preventing wall acidification. 

CSV responds to chromiumlV/) as well as to (///) but the response to chromium(///) diminishes rapidly with time approaching zero after about 15 min due to chromium(///) adsorption on the cell wall. Thereafter the response is due to chromium(V/) only. For this reason it is recommended to convert all chromium into the V7 state prior to the analysis. The only way to prevent the chromium(//7) signal from diminishing is to use a flow cell instead of the standard, batch, voltammetric cell. This adsorption is not special to voltammetry the chromium(///) adsorbs readily on almost anything, and its rapid removal from water samples is normally prevented by acidification. Acidification causes all chromium(V7) to... 

Cell-wall loosening and a concomitant increase of growth rate can be elicited by acidification. It is assumed that auxin stimulates a plasma membrane H+-ATPase that causes the acidification. A lateral translocation of auxin during unilateral irradiation would thus lead to differential acidification and thus differential growth. In Zea coleoptiles, auxin enhances the exocytosis and the synthesis of H+-ATPase of the plasma membrane, and also the activation of existing H+-ATPase was demonstrated. The strong and critical points of this so-called acid-growth theory were discussed. ... 

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