Changes in microvilli and Golgi-associated membranes of lepidopteran cells induced by an insecticidally active bacterial δ-endotoxin

1989 ◽  
Vol 93 (2) ◽  
pp. 337-347
Author(s):  
NANCY J. LANE ◽  
J. B. HARRISON ◽  
W. M. LEE

The δ-endotoxin from Bacillus thuringiensis var. kurstaki was fed to late larvae of the tobacco hornworm, Manduca sexta, to determine its effect on the anterior midgut epithelium, which was examined ultrastructurally at intervals thereafter. The cells of the midgut are primarily of the columnar and goblet variety and the effects of the toxin were more pronounced on the former. Tissues examined after only 1–5 min of exposure to the toxin already revealed fine-structural alterations. These were most notably changes in the microvilli and membranes associated spatially with the Golgi complex: vacuoles associated with its maturing face became enlarged. This effect was intensified with more-extensive exposure to the toxin, resulting in an increase in both vacuoles and the number of lysosomal bodies, many containing myelin-like formations; some of these arose as autophagic vacuoles. There seemed to be no consistent increase in endocytotic activity at the apical border, however. The intramembranous particle population of the microvilli of the columnar cells showed some slight changes with toxin treatment; alterations in microvillar contours also occured. The intercellular septate and gap junctions on the lateral borders were sometimes disrupted and with time often became internalized. It seems, then, that the toxin initially modifies the microvillar membranes and subsequently the Golgi-associated saccules are affected, giving rise to vacuoles and lysosomes.

Author(s):  
Ji-da Dai ◽  
M. Joseph Costello ◽  
Lawrence I. Gilbert

Insect molting and metamorphosis are elicited by a class of polyhydroxylated steroids, ecdysteroids, that originate in the prothoracic glands (PGs). Prothoracicotropic hormone stimulation of steroidogenesis by the PGs at the cellular level involves both calcium and cAMP. Cell-to-cell communication mediated by gap junctions may play a key role in regulating signal transduction by controlling the transmission of small molecules and ions between adjacent cells. This is the first report of gap junctions in the PGs, the evidence obtained by means of SEM, thin sections and freeze-fracture replicas.


Development ◽  
1989 ◽  
Vol 106 (4) ◽  
pp. 691-705 ◽  
Author(s):  
C. Tickle ◽  
A. Crawley ◽  
J. Farrar

Local application of retinoic acid to wing buds of chick embryos leads to dose- and position-dependent changes in the pattern of cellular differentiation. Early effects of retinoid treatment on the apical ectodermal ridge coordinate pattern changes and morphogenesis. The length of the apical ridge increases when additional digits will form but decreases when digits are lost. These changes in length can be understood in terms of a threshold response to the local retinoid concentration that results in either disappearance or maintenance of the ridge (Lee & Tickle, J. Embryol. exp. Morph. 90, 139–169 (1985)). Here, we have analysed the mechanisms involved in ridge disappearance by locally applying retinoic acid to the apex of stage 20 chick wing buds. With this treatment regime, low doses give duplicated digit patterns and higher doses truncations. The height of the apical ridge is progressively reduced with increasing doses of retinoid and the time course of ridge flattening indicates that the height of the ridge is correlated with bud outgrowth. With high doses of retinoic acid, the typical ridge, a pseudostratified epithelium in which the columnar cells are tightly packed, disappears and the epithelium at the tip of the bud consists of loosely packed cuboidal cells. Shortly after treatment, there is a decrease in the number of gap junctions between ridge cells. This early change in cell contacts suggests that gap junctions may be involved in maintaining epithelial morphology. When treated epithelium is recombined with untreated mesenchyme, an apical ridge is reestablished and distal structures can be generated. In contrast, when treated mesenchyme is recombined with the epithelium from normal buds, only proximal structures are formed. Therefore, retinoids can lead to a reorganization of the apical ectodermal ridge which is mediated and maintained by the mesenchyme.


1985 ◽  
Vol 74 (1) ◽  
pp. 137-152
Author(s):  
B.L. Gupta ◽  
J.A. Dow ◽  
T.A. Hall ◽  
W.R. Harvey

An alkaline hydrolysate of Bacillus thuringiensis var kurstaki HD1 (Btk) parasporal crystals was administered at 25 micrograms ml-1 (f.c.) to isolated, short-circuited, midguts of tobacco hornworm (Manduca sexta) larvae. The short-circuit current (s.c.c.), a precise measure of K+ active transport, was inhibited by 78% in 10 min in Btk-treated midguts as compared to controls. The elemental concentrations of K, together with Na, Mg, P, S, Cl and Ca, as well as the water content, were determined by electron probe X-ray microanalysis (EPXMA) in the muscle cells, columnar cells and goblet cells, as well as in the extracellular goblet cavity and the bathing media. The average K concentration in the goblet cell cavity was 129 mmol/kg wet wt in control midguts but only 37 mmol/kg wet wt in Btk-treated midguts. The elemental concentrations, including that of K, in other cell compartments were much less affected by Btk, but a rise in total cell calcium is suggested. It has been previously suggested that in vitro Btk acts specifically on limited regions of the apical membrane of the midgut epithelial cells. The simplest interpretation of the EPXMA results would be that initially Btk interacts specifically with the goblet cell apical membrane, which bounds the goblet cavity and contains the K+ pump responsible for the s.c.c. and high transepithelial potential difference (p.d.). Such interaction results in a rapid disruption of K+ transport across the goblet cell apical membrane, leading to dissipation of the K+ gradient and loss of p.d. The histopathological changes previously reported by other workers would then be a consequence of K+ pump inhibition causing changes in the intracellular pH, Ca2+ etc. Some possible molecular bases for these specific interactions between Btk and cell membrane are discussed.


2010 ◽  
Vol 1798 (6) ◽  
pp. 1111-1118 ◽  
Author(s):  
Jean-Frédéric Brunet ◽  
Vincent Vachon ◽  
Marc Juteau ◽  
Jeroen Van Rie ◽  
Geneviève Larouche ◽  
...  

1997 ◽  
Vol 256 (5) ◽  
pp. 517-524 ◽  
Author(s):  
S. E. Franklin ◽  
L. Young ◽  
D. Watson ◽  
A. Cigan ◽  
T. Meyer ◽  
...  

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