Abstract
The nuclear pore complex (NPC) is the sole gateway to the nuclear interior, and its function is essential to all eukaryotic life. Controlling the functionality of NPCs is a tremendous challenge for cells. Firstly, NPCs are large structures, and their complex assembly does occasionally go awry. Secondly, once assembled, some components of the NPC persist for an extremely long time and, as a result, are susceptible to accumulate damage. Lastly, a significant proportion of the NPC is composed of intrinsically disordered proteins that are prone to aggregation. In this review, we summarize how the quality of NPCs is guarded in young cells and discuss the current knowledge on the fate of NPCs during normal aging in different tissues and organisms. We discuss the extent to which current data supports a hypothesis that NPCs are poorly maintained during aging of nondividing cells, while in dividing cells the main challenge is related to the assembly of new NPCs. Our survey of current knowledge points toward NPC quality control as an important node in aging of both dividing and nondividing cells. Here, the loss of protein homeostasis during aging is central and the NPC appears to both be impacted by, and to drive, this process.
Highlights
One of the nine described universal hallmarks of aging is the loss of protein homeostasis [1]
The yeast mother cells and the differentiated cells both are both mortal and retain damaged components [54,57,58,59,60]. These general considerations of how yeast replicative and chronological aging may relate to aging in rodent tissues are somewhat reflected in the analysis of age-related changes of nuclear pore complex (NPC) components as follows: The age-related changes in Nup abundances in yeast replicative aging correlate with those in aged rat liver, where the shared loss of the basket Nups is the main contributor to this correlation being significant (Fig. 3E)
One explanation for the reduced number of NPCs in the liver of aged rats is, that the postmitotic assembly of NPCs might be an opportunity for cells to clear up substoichiometric protein complexes, in line with this interpretation is the low interquartile region (IQR) of the aged rat liver sample (Fig. 3)
Summary
Poor old pores-The challenge of making and maintaining nuclear pore complexes in aging Rempel, Irina L.; Steen, Anton; Veenhoff, Liesbeth M. Poor old pores-The challenge of making and maintaining nuclear pore complexes in aging. More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverneamendment. We discuss the extent to which current data supports a hypothesis that NPCs are poorly maintained during aging of nondividing cells, while in dividing cells the main challenge is related to the assembly of new NPCs. Our survey of current knowledge points toward NPC quality control as an important node in aging of both dividing and nondividing cells. The loss of protein homeostasis during aging is central and the NPC appears to both be impacted by, and to drive, this process
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
