Structure of the Golgi apparatus in stimulated and nonstimulated acinar cells of mammary glands of the rat

Abstract

The structural features of the Golgi apparatus of acinar cells of mammary glands were examined with the electron microscope in 3 groups of rats: (1) in lactating female animals at 8 days postpartum, which served as controls; (2) in female rats sacrificed at various intervals from 2 to 30 hours following separation from their 8-day old pups; and (3) in females separated from their 8-day-old pups for a period of 12 hours and returned to their litters for durations of 1, 2, 4, and 8 hours. In animals of group 2, the Golgi stacks remained identical to that of controls between 2 and 8 hours. At 12 hours and later, the Golgi stacks decreased progressively in size, but the number of elements composing the stacks remained similar to that of lactating females and all contained casein submicelles. At 24 and 30 hours, typical secretory granules containing casein micelles disappeared from the trans aspect of the stacks. The earliest and most striking changes observed in the Golgi apparatus of the rats of group 2 took place at 12 hours. At this time, the prosecretory and secretory granules decreased considerably in volume and lost most of their electron-lucent content. This indicated that the delivery of small molecules, i.e., lactose and H2O, to these structures was soon altered following arrest of the sucking stimulus. In animals of group 3, the size of prosecretory and secretory granules and the amount of their electron-lucent content reverted to normal at 4 hours. Thus the influx of lactose and H2O into these structures appears to be rapidly restored after returning the pups to their mothers. The decrease in size of the Golgi stacks noted at 12, 18, and 24 hours following arrest of lactation (group 2), was accompanied by an increase in number of small vesicles that formed clusters next to the Golgi stacks and in "wells." Thus in these regressing Golgi stacks, many of the associated small vesicles appear to arise by vesiculation of the saccules.

The Biogenesis of the Golgi Ribbon: The Roles of Membrane Input from the ER and of GM130

“…However, as soon as this input of membranes from the ER is slowed down or interrupted, this ribbon undergoes disconnection into isolated Golgi stacks with shorter cisternae (see Figure 9). This thus provides a further example of the high degree of plasticity of the GC, which undergoes an extensive remodeling that is dependent on its level of activity and the developmental stage of the cell (Jasmin et al, 1989;Clermont et al, 1993;Marsh et al, 2004;Trucco et al, 2004).…”

“…Different subcompartments of the GC can vary in volume according to their rates of membrane input and output (Griffiths et al, 1989;Clermont et al, 1993;Morin-Ganet et al, 2000); however, it is unclear how this flux of membranes impacts on the organization of the Golgi ribbon itself. To address this issue, different experimental conditions were set up to interrupt the arrival of EGCs at the GC and to analyze the effects of this block (and of its removal) on the ultrastructure of the GC.…”

Architecture of the Mammalian Golgi

“…Within a given cell type, the Golgi volume depends on the level of protein synthesis. Inhibition of ER to Golgi traffic can lead to the disappearance of the Golgi (Lee and Linstedt 1999;Glick 2000;MorinGanet et al 2000;Prescott et al 2001), whereas an increase in synthesis can lead to increased Golgi volume (Clermont et al 1993;Noske et al 2008). The Golgi adapts to these changes by Golgi-based signaling systems (Farhan and Rabouille 2011), for example, by monitoring protein chaperones that escape the ER.…”

Milk lipid secretion: recent biomolecular aspects

“…Significantly, there is marked ER expansion during mammary gland differentiation (19–21), and in species in which it has been studied, the ER accounts for approximately 25% of the total volume of mammary epithelial cells in lactating animals (21). Thus, CLD production by ER processes may represent a regulatory step in the overall rate by which lipids are transferred into milk.…”