The effects of potassium deficiency (KD) and all-macronutrient deficiency (MD) on elongation of tap and lateral roots were studied on maritime pine seedlings (Pinus pinaster Ait.) in hydroponic culture.

Tap root elongation was unaffected by either of the two deficiencies. By marked contrast, lateral root elongation was strongly reduced. The analyses of cell turgor pressure and relative elemental growth rate (REGR) profile in the growing zone allowed us to determine the effects of the nutrient stresses on cell-wall properties. For both deficiency treatments, elongation rate, REGR profile (measured only for control and KD) and turgor pressure in the fastest growing cells were unaffected in the tap root, suggesting that KD and MD did not modify cell-wall properties in the growing zone. In lateral roots, KD shortened the growing zone and significantly reduced REGR. However, turgor pressure remained unaffected in this region. The absence of turgor pressure change suggests that KD reduced elongation of lateral roots by tightening cell walls. In mature cells of the two types of roots, turgor and osmotic pressures tended to be reduced by the nutrient deficiencies, indicating that these parameters were better maintained in the growing cells.

Cell turgor and osmotic pressures of control plants were 0·1 MPa lower at 30 mm (mature cells) than at 2–4 mm (expanding cells) from the meristem. Moreover, these parameters were 0·1 MPa lower in expanding cells of lateral roots than in those of tap the root. Turgor and osmotic pressures were not homogeneous throughout the root system and were affected differently by the nutrient deficiencies depending on the location in the root system.

The effects of potassium deficiency on growth, K content and protein synthesis have been compared in 4–13-week-old rats. When maintained on K-deficient fodder (1 mmol/kg) rats ceased to grow within a few days, and the incorporation of [3H]leucine into skeletal muscle protein in vivo was reduced by 28–38%. Pair-feeding experiments showed that this inhibition was not due to reduced energy intake. Following 14 d on K-deficient fodder, there was a further reduction (39–56 %) in the incorporation of [3H]leucine into skeletal muscle protein, whereas the incorporation into plasma, heart and liver proteins was not affected. The accumulation of the non-metabolized amino acid α-aminoisobutyric acid in the heart and skeletal muscles was not reduced. The inhibitory effect of K deficiency on 3H-labelling of muscle protein was seen following intraperitoneal (10–240 min) as well as intravenous (10 min) injection of [3H]leucine. In addition, the incorporation of [3H]phenylalanine into skeletal muscle protein was reduced in K-depleted animals. Following acute K repletion in vivo leading to complete normalization of muscle K content, the incorporation of [3H]leucine into muscle protein showed no increase within 2 h, but reached 76 and 104% of the control level within 24 and 72 h respectively. This was associated with a rapid initial weight gain, but normal body-weight was not reached until after 7 weeks of K repletion. Following 7 d on K-deficient fodder the inhibition of growth and protein synthesis was closely correlated with the K content of the fodder (1–40 mmol/kg) and significant already at modest reductions in muscle K content. In vitro experiments with soleus muscle showed a linear relationship between the incorporation of [3H]leucine into muscle protein and K content, but the sensitivity to cellular K deficiency induced in vitro was much less pronounced than that induced in vivo. Thus, in soleus and extensor digitorum longus (EDL) muscles prepared from K-deficient rats, the incorporation of [3H]leucine was reduced by 30 and 47 % respectively. This defect was completely restored by 24 h K repletion in vivo. It is concluded that in the intact organism protein synthesis and growth are very sensitive to dietary K deficiency and that this can only partly be accounted for by the reduction in cellular K content per se. The observations emphasize the need for adequate K supplies to ensure optimum utilization of food elements for protein synthesis and growth.