The Hayflick Limit

2021 ◽  
Vol 22 (2) ◽  
pp. 107-111
Author(s):  
Jessica Franken
Keyword(s):  
1984 ◽  
Vol 9 (1) ◽  
pp. 49-65 ◽  
Author(s):  
Rita B. Effros ◽  
Roy L. Walford
Keyword(s):  
T Cell ◽  

2021 ◽  
Author(s):  
◽  
Euan Russell

<p>Gram-negative bacteria produce outer-membrane vesicles (OMVs) that have biological roles ranging from biofilm formation, modulation of host-cell interactions & delivery of virulence factors. Several studies have shown a role for OMVs to act as intracellular signals to co-ordinate the behaviour of bacteria. This study showed OMVs generated at sub-lethal ciprofloxacin concentrations were capable of programming naïve P. aeruginosa cultures resulting in premature entry into stationary-phase and a significantly lower final culture density reached after 14 hrs. Pyoverdine production was also initiated after 6 hrs in cultures treated with OMVs.  Heat-inactivation of OMVs failed to impede OMV-mediated growth inhibition & pyoverdine production. Chloroform-disruption of OMVs prevented OMV-mediated growth inhibition but did not inhibit OMV-induced pyoverdine production. It is likely that these effects are mediated by multiple signals as opposed to a single mechanism. This suggests that a protein is not responsible for OMV-mediated growth inhibition and an intact OMV lipid bilayer is required. Induction of pyoverdine production is likely due to a lipid (such as a homo-serine lactone) or small molecule present within OMVs.  Preincubation with OMVs for 2-4 hrs resulted in a substantial decrease in the final culture density from cultures that were exposed to OMVs during the course of growth. This suggests that OMV fusion is capable of programming naïve bacteria to set a predetermined division limit on subsequent daughter cells. We coin this as the ‘Dayflick’ limit due to the similarities of the Hayflick limit in eukaryotic cells.  This shows that OMVs act as intercellular messaging vehicles between bacteria that communicate and program naïve bacteria to adapt to the environment under which they were generated in, aiding survival in harsh environments. Further study is needed to determine what OMV components are responsible for initiating these responses and to determine how long the programming is stable.</p>


2017 ◽  
Vol 216 (5) ◽  
pp. 511-513
Author(s):  
Paul D Griffiths
Keyword(s):  

Gerontology ◽  
2017 ◽  
Vol 64 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Zoe Gill ◽  
Martin Nieuwoudt ◽  
Wilfred Ndifon

The adaptive immune system (AIS) acquires significant deficiency during chronological ageing, making older individuals more susceptible to infections and less responsive to vaccines compared to younger individuals. At the cellular level, one of the most striking features of this ageing-related immune deficiency is the dramatic loss of T-cell diversity that occurs in elderly humans. After the age of 70 years, there is a sharp decline in the diversity of naïve T cells, including a >10-fold decrease in the CD4+ compartment and a >100-fold decrease in the CD8+ compartment. Such changes are detrimental because the AIS relies on a diverse naïve T-cell pool to respond to novel pathogens. Recent work suggests that this collapse of naïve T-cell diversity results from T cells reaching the Hayflick limit and being eliminated through both antigen-dependent and -independent pathways. The progressive attrition of telomeres is the molecular mechanism that underlies this Hayflick limit. Therefore, we propose that by measuring the telomere lengths of T cells with high resolution, it is possible to develop a unique biomarker of immune deficiency, potentially much better correlated with individual susceptibility to diseases compared to chronological age alone.


Author(s):  
Stephen S. Hal

Of the countless interviews I have conducted with scientists over the years, only once has a question prompted something of a striptease. In December of 1999, I found myself in the elegant parlor of the Union Club in New York City, chatting with a biologist named Leonard Hayflick. Although hardly a household name to the general public, Hayflick is that rare scientist whose name is permanently attached to a biological phenomenon. It is known as the “Hayflick limit,” and it derives from experiments he did in the late 19505 and early 19605 showing that human cells grown in Petri dishes will predictably replicate for a certain number of cell divisions, but then hit a wall and stop dividing. This has obvious implications for cell biology, aging, and immortality (of the in vitro sort), and indeed the Hayflick limit has been the seed around which a spirited biological debate about the biology of aging has swirled, without definitive resolution, for about four decades now. Because of this history, Hayflick has closely followed the recent work on the biology of aging and regenerative medicine, which in turn has made him a front-row spectator in the more recent controversies involving human embryonic stem cell research and “therapeutic cloning.” At the time of my conversation with Hayflick, his longtime friend Michael West was attempting to obtain human embryonic stem cells through cloning—in a particularly controversial way, by putting human cells into egg cells from ... cows. Almost as an aside, I asked Hayflick what he thought about West's experiments. Hayflick replied by rolling up his pants leg. He bared enough skin to be able to point out a tiny dimple on his right knee. “The human cells he's using for the cow work came from here,” he said. I had to stand up and lean over to see it, but there was undeniably a tiny divot in Hayflick's skin. The implications were stunning: Leonard Hayflick, the father of cellular senescence and one of the elder statesmen of gerontology, was allowing himself, in a manner of speaking, to be cloned. In addition to making the obvious point that even the most innocuous question can elicit a startling answer, Hayflick's reply offered another lesson, too: that colorful characters can provide a narrative thread for bringing a controversy to life.


2015 ◽  
Vol 25 (3) ◽  
pp. 240-242 ◽  
Author(s):  
Friedrich C. Luft
Keyword(s):  

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