Production and biochemical characterization of polygalacturonases produced byAureobasidium pullulans from forest soil

The production of individual form of extracellular polygalacturonase byAureobasidium pullulans from forest soil was found to depend on the pH of cultivation medium as well as on the nitrogen source in the precultivation or cultivation medium. Polygalacturonases were purified and characterized. The pH optima of polygalacturonases produced in the first phases of cultivation (24 or 48 h) and after 10 days as well as their molecular masses, isoelectric points, action pattern and ability to cleave polymeric and oligomeric substrates were different. Generally, polygalacturonases with random action pattern (EC 3.2.1.15) were produced only in the first phases of cultivation in acidic medium. The function of these enzymes for A.pullulans in the colonization of plant material rather than in the destruction of plant was hypothesized in physiological conditions. Exopolygalacturonases (EC 3.2.1.67) with terminal action pattern were produced in later phases of growth. Oligogalacturonate hydrolase as well as strongly basic polygalacturonase with unusual action pattern on substrates were found.     

The life style of Aureobasidium pullulans and the multiple forms of its polygalacturonase

The life style of Aureobasidium pullulans on pectin medium and its production of extracellular polygalacturonases are closely related. Polygalacturonases with random action pattern (EC 3.2.1.15) were formed in the first phases of cultivation, whereas exopolygalacturonases (EC 3.2.1.67) with terminal action pattern on pectin were produced during the whole growth of this yeast-like fungus. The production and inactivation of individual enzyme forms during cultivation were strongly dependent on the pH value of the pectin medium. Various kinds of stress can support the prolongation of the phase of endo-acting enzyme production, as well as the increase of their activity.     

Variable Cell Lineages form the Functional Pea Epidermis

Evidence was sought for cellular programs and cellular interactionsacting during the formation of stomatal spacing patterns. Dailyreplicas of the surfaces of Pisum sativum leaves were used toreconstruct the cellular development of specific regions ofthe epidermis. During the period studied small primordia becamemature leaves; this involved a 250-fold increase in area anda 20-fold increase in cell number. The earliest event correlatedwith the development of a stoma was an unequal division, andsuch divisions were common in neighbouring and even within thesame cells. A distinct cell lineage started with these unequaldivisions, forming both a stoma and most of the cells that separatedit from its neighbours. Both products of an unequal divisionbecame regular epidermal cells only where such development preventedthe formation of two stomata that would have been in directcontact with one another. Neighbouring stomata often developedand matured together, indicating that there was no mutual inhibitionbetween developing stomata that were more than one cell apart.It is concluded that stomata are products of an intracellularprogram which generates stomatal patterns during rather thanpreceding development. This program can be modified and evenstopped during its entire course, allowing for the correctionof local ‘mistakes’ of stomatal patterning. Cell lineages, cell determination, cellular interactions, epidermal development, garden peas, immature stomata, pattern formation, Pisum sativum, spacing patterns, stomata, unequal divisions     

Effect of glucose utilization inhibitor isolated from the serum and urine of patients with chronic renal failure on the free fatty acid metabolism in rat kidney cortex slices.

The authors studied interference by the inhibitor of glucose utilization with free fatty acid (FFA) metabolism in rat kidney cortex slices. They found that FFA uptake by the kidneys, their incorporation into triglycerides (TG) and oxidation to 14CO2 were lower when the inhibitor was present in the incubation medium. The findings show that the inhibitor, as well as inhibiting glucose utilization in various tissues, interferes directly with fat metabolism.