No abstract

FUSEE, M. C., et J. M. LEATHERWOOD. 1972. Regulation of cellulase from Rln~ri~rococcrrs. Can. J.Microbiol. 18: 347-353. On a examine la regulation de la cellulose chez Rr~lninococcrrs nlbrrs et R. flavefacielu. L'hydrolyse de la cellulose, cornme mesuree par la for~nation des zones claires autour des colonies bacteriennes qui se developpent sur cellulose gelosee en tubes enrobes, est inhibee par des niveaux moyens de cellobiose. U n intermediaire dans le n~etabolisme de la cellobiose peut Ctrc responsable de I'inhibition parce que des lignees qui peuvent ~~tiliser le sucrose ou le glucose sont similairement inhibees par ces sources d'energie. L'inhibition de la cellulose a ete etudiee en relation soit de la repression de la synthkse de l'enzyme, soit de I'inhibition de I'activitC enzymatiq~~e par les produits. 1 1 n'y a aucune inhibition par la cellobiose ajoutte soit au milieu d'essai enzymatique de routine soit au milieu d'essai dont des faibles concentrations de carboxymethylcellulose sont utilisees. Un mecanis~ne de repression est indiqut par la diminution de I'activite specifique des cultures qui se sont developpees en presence de fortes concentrations de cellobiose. L'activite specifique a Cte calculee comme Ctant I'activitk enzy~natiq~~e sur le carboxymCthylcellulose en regard de la croissance des cellules. Le mecanis~ne de repression n'a pas ete differentie du model propose par Jacob et Monod et de la repression par les catabolites. Rr~~~zi~~ococcrr~ nlbrrs, cultive dans un milieu liquide de cellulose et de cellobiose, ~nontre un mode de croissance diauxique semblable a celui decrit par Monod. FUSEE, M. C., and J. M. LEATHERWOOD. 1972. Regulation of cellulase from Rrm~i~~ococcus. Can. J.Microbiol. 18: 347-353. The regulation of cellulase was examined in Rrrl?~i~lococcrrs albrls and R. flavefacietu. Hydrolysis of cellulose, as shown by the formation of clear zones around the colonies of bacteria grown in celluloseagar roll tubes, was inhibited by moderate levels of cellobiose. An intermediate in the metabolism of cellobiose may be responsible for the inhibition since strains which can use either sucrose or lactose were similarly inhibited by these energy sources. The inhibition of cellulase was examined in relation to either repression of enzyme synthesis or product inhibition of the enzyme activity. There was no inhibition by cellobiose added either to the routine enzymatic assay or to assays using low concentrations of carboxymethylcellulose. Arepression mechanism was indicated by the decrease in specific activity of cultures grown in higher concentrations of cellobiose. The specific activity was calculated as the enzymatic activity oncarboxyn~ethylcellulose with respect to cell growth. The mechanism of repression was not distinguished between the model proposed by Jacob and Monod and catabolite repression. The growth of R. albrrs cultured in cellobiose-cellulose liquid medium exhibited a diauxic pattern similar to that described by Monod.As early as 1932, Sarles et al. (24), working with thermophilic ce...

A Cellulomonas sp. was isolated from the soil which hydrolyzed cellulose, as shown by clear-zone formation on cellulose agar medium. Catabolite repression of cellulase synthesis occurred when moderate levels of glucose were added to the medium. A stable mutant that no longer exhibits catabolite repression was produced through treatment of the wild-type organism with N-methyl-N '-nitro-N-nitrosoguanidine. Both enzyme concentration and specific activity, as determined by the rate of hydrolysis of carboxymethylcellulose, were greater with the mutant than with the wild-type organism under various test conditions. The wild type had no measurable cellulase activity when grown in the presence of either 1.0% glucose or cellobiose. Cellobiose, but not glucose, inhibited enzyme activity towards both cellulose and carboxymethylcellulose. Cellobiose, cellulose, and sophorose at low concentrations induced cellulase synthesis in both the wild-type and the mutant organism. Cellulase regulation appears to depend upon a complex relationship involving catabolite repression, inhibition, and induction.

Male mice from a line selected for rapid postweaning growth (M16) and an unselected control (ICR) were reared from birth to 3 weeks either in litters of eight (N8) or 14 (N14). Body weight gain and feed intake of M16 mice were greater than ICR. These high rates of gain and feed intake also were extended to an older age in M16 (10 weeks) than in ICR (6 weeks). The M16 line exceeded the ICR line and N8 mice exceeded N14 for fat, lean, ash, and live body weights at 4, 6, 10, 16, and 30 weeks of age. Fat percentage was greater in N8 than N14 for both ICR and M16. The adipose cellularity of the epididymal fat pads of M16 indicated a hypertrophic-hyperplastic form of obesity at 10, 16, and 30 weeks. Within each line, the N14 mice had fewer and slightly smaller fat cells than N8. However, M16-N14 mice still had considerably more and larger fat cells than ICR-N8. Restriction of energy intake from birth to 3 weeks reduced subsequent feed intake and degree of obesity. After 4 weeks, the genetic effect exerted a greater influence on the development of obesity than the preweaning nutritional regimen.

The M16 line of mice, selected for rapid postweaning gain, exhibits polygenically controlled obesity and hyperphagia. The effect of limiting postweaning energy intake on the subsequent growth and development of obesity in M16 mice was investigated. Male mice from M16 and an unselected line (ICR) were provided either ad libitum or limited (congruent to 70% of ad libitum) feed during the rapid postweaning growth period from 4 to 6 weeks of age. Body weights (g) at 6 weeks of age were: ad libitum ICR (31.0 +/- 0.6), restricted ICR (23.8 +/- 0.7), ad libitum M16 (45.0 +/- 0.6) and restricted M16 (30.1 +/- 0.6). In both lines, restricted feed intake severely depressed body fat, lean, ash, and water at 6 weeks. In addition, percent triacylglycerol, fat cell size and number in the epididymal fat pads were lower. Restricted M16 and ICR mice showed a marked compensatory gain in all body components when subsequently fed ad libitum for 10 weeks. All measurements of adiposity at 16 weeks were similar for the restricted and ad libitum regimens within each line. The relative amounts of energy deposited as fat and lean between 4 and 16 weeks were not influenced by restricted feeding, but M16 mice deposited a larger proportion of energy as fat than as lean when compared with ICR mice. The results suggest that fat cell number is determined at a relatively early age in mice and is primarily under genetic control.