Morphometry of nuclear pore complexes in thyroid cells during hyperplasia and involution

doi:10.1016/0303-7207(81)90065-4

Molecular and Cellular Endocrinology

Volume 23, Issue 2, August 1981, Pages 137-149

https://doi.org/10.1016/0303-7207(81)90065-4 Get rights and content

Abstract

Nuclear pore complexes were analyzed in freeze-fractured replicas of thyroid follicular cells of C₃H mice in different physiological states. Thyroid stimulation induced a rapid and simultaneous increase of the nuclear surface and volume and of the total number of pore complexes. The numerical density (N_a) of pore complexes increased at the 6th day of stimulation, but after that time the proportion of cells with an increased N_a was always higher than the proportion of ³H-labelled nuclei. During thyroid involution, all the nuclear parameters, including the N_a, returned to normal values.

These results indicate that the total number of pore complexes and their N_a are correlated with the cellular activity rather than with the cell cycle. They also suggest that 2 different mechanisms are involved in the generation of pore complexes: first, an addition of new memranes with a low density of pore complexes; later, a formation of new pore complexes in preexisting membranes. However, during involution, parts of the nuclear membranes and pore complexes in the remaining parts disappear synchronously.

In freeze-fractured thyroid nuclear membranes, 2 neighbouring pore complexes were always separated by a distance of 105 nm. Clusters of pore complexes were not observed. A comparison of the distances between pore complexes and between randomly generated points never showed any significant differences indicating that pore complexes were randomly distributed.

References (33)

D. Branton et al.
J. Ultrastruct. Res.
(1964)
C.M. Feldherr
Tissue Cell
(1971)
W.W. Franke et al.
J. Ultrastruct. Res.
(1970)
W.W. Franke et al.
J. Markovics et al.
Exp. Cell Res.
(1974)
A. Taurog
Rec. Progr. Hormone Res.
(1970)
D.J. Teigler et al.
Tissue Cell
(1972)
P. Baudhuin et al.
J. Cell Biol.
(1967)
P. Baudhuin et al.
J. Microsc.
(1979)
G.A. Bray
J. Clin. Invest.
(1968)

P.J. Clark et al.

Ecology

(1954)

L.M. Cruz Orive

J. Microsc.

(1976)

J.-F. Denef et al.

Histochemistry

(1979)

E.J. Du Praw

C.M. Feldherr

J. Cell Biol.

(1969)

W.W. Franke

J. Cell Biol.

(1966)

Cited by (13)

Nuclear pore complex maintenance and implications for age-related diseases
2022, Trends in Cell Biology
Citation Excerpt :
Nevertheless, since all NPCs will be disassembled from the mother cells and equally reassembled in each daughter cell, the number of newly assembled NPCs during interphase is strictly regulated to maintain proper NPC amount after cell division. Dysregulation of the NPC number can cause severe outcomes, including cell identity loss and even tumorigenesis [33,34]. A recent study has shown that regulation of the interphase assembly exists when the Nup107–160 subcomplex is recruited to Pom121/Nup153.
Nuclear pore complexes (NPCs) bridge the nucleus and the cytoplasm and are indispensable for crucial cellular activities, such as bidirectional molecular trafficking and gene transcription regulation. The discovery of long-lived proteins (LLPs) in NPCs from postmitotic cells raises the exciting possibility that the maintenance of NPC integrity might play an inherent role in lifelong cell function. Age-dependent deterioration of NPCs and loss of nuclear integrity have been linked to age-related decline in postmitotic cell function and degenerative diseases. In this review, we discuss our current understanding of NPC maintenance in proliferating and postmitotic cells, and how malfunction of nucleoporins (Nups) might contribute to the pathogenesis of various neurodegenerative and cardiovascular diseases.
Poring over chromosomes: mitotic nuclear pore complex segregation
2019, Current Opinion in Cell Biology
Citation Excerpt :
NPC number per nucleus is controlled in a cell-type-specific and organism-specific manner, ranging from between a few hundred in yeast to a few thousands in mammalian cells [2,3]. Failure to control NPC numbers is associated with aggressive tumors and thyroid hyperplasia [4,5] but despite its importance, mechanisms regulating NPC number remain poorly understood. Once assembled into the NE, NPCs are stable structures that persist throughout interphase [6] and knockdown of proteins involved in NPC assembly results in an overall reduction in NPC numbers in yeast and humans [7,8].
Eukaryotic cells rely on flux of macromolecules between the nucleus and the cytoplasm for growth and survival. Bidirectional transport is achieved through Nuclear Pore Complexes (NPCs) embedded in the Nuclear Envelope (NE). NPC proteins perform other cellular functions during mitosis, chromatin organization, DNA repair and gene regulation. Dysregulation of NPC number, or defects in their structure and function, are linked to numerous diseases but how NPCs are faithfully inherited during mitosis is poorly understood. In this review, we discuss recent insights to mechanisms of mammalian mitotic NPC segregation and NPC assembly as well as mitotic NPC inheritance via the mitotic chromatin located NPC protein Nup2 in Aspergillus nidulans. We suggest mitotic Nup2 chromatin-based mechanisms could also operate in vertebrate cells.
Testosterone-induced changes in nuclear pore complex number of prostatic nuclei from castrated rats
1982, Journal of Ultrasructure Research
The time-course effect of testosterone on nuclear pore formation was studied in ventral prostate isolated nuclei from castrated rats. The pore density was determined by the freeze-etching technique and electron microscopy; the nuclear envelope surface area was estimated by phase-contrast microscopy. The first detectable changes occurred 1 day after hormone stimulation and consisted of an increase in nuclear surface with a consequent increase in the total number of pores per nucleus although the pore density remained statistically unchanged. Again, between the second and third days of stimulation the pore density remained unchanged, while total pore number increased due to an increase of nuclear surface. These results show that the pore density variations are partly independent of additional nuclear membrane synthesis. Nuclear pore-density increase was found to present a biphasic pattern that correlates with the rate of DNA replication and mitosis known to be stimulated in these cells by testosterone. The progressive increase in both pore number and density beyond the periods of maximal cell division, however, is best related to the stimulation of the cell metabolism.
Quantitative analysis of nuclear pore complex organization in Schizosaccharomyces pombe
2022, Life Science Alliance
Quantitative analysis of nuclear pore complex organization in Schizosaccharomyces pombe
2021, bioRxiv
The nuclear pore complex and mrna export in cancer
2021, Cancers

View all citing articles on Scopus

View full text

Morphometry of nuclear pore complexes in thyroid cells during hyperplasia and involution

Abstract

J. Ultrastruct. Res.

Tissue Cell

J. Ultrastruct. Res.

Exp. Cell Res.

Rec. Progr. Hormone Res.

Tissue Cell

J. Cell Biol.

J. Microsc.

J. Clin. Invest.

Ecology

J. Microsc.

Histochemistry

J. Cell Biol.

J. Cell Biol.