(1) ‘….we expected the effect of delaying reproduction among paternal and maternal grandfathers to be equal in size and half as strong as the effect of a comparable delay in paternal age at reproduction. Contrary to this expectation, we found that the effect size of the paternal grandfather’s age on their grand-children’s TL was larger than the effect of the maternal grand-father’s age at the mother’s birth on the grandchild’s TL….’
This finding is particularly interesting when we consider the standard Mendelian model of inheritance, where it is expected that half an individuals’ nuclear genetic material comes from each parent, (additionally we can extrapolate that a quarter of this same genetic material comes from each of a person’s four grandparents). However in this study it was observed that the paternal grandfather’s age at the father’s conception had a disproportionate effect (heritability) on TL.
How can this finding be explained? It is not the first time that this has been observed in the inheritance of TL. A 2007 study found exactly the same trend, and some hypotheses have been presented to explain the phenomenon. Specifically the activity of telomere protection proteins are thought to play an important role.
(2) ‘Together with this evidence, our findings lead us to the prediction that being born into a lineage in which recent male ancestors, particularly patrilineal ancestors, reproduced at later ages could have long-term health benefits….’
What exactly are the health benefits associated with TL? The most commonly cited is increased cell lifespan which in turn has an impact on general health and survival. However, as stated in the original study, the association between TL and cancer development risk is still unclear. Given this preliminary position, it seems premature to make the conclusion stated above. Importantly TL should not be viewed simply as the limiting factor in cell life span but also as a possible regulatory factor associated with necessary cell senescence as a result of accumulated somatic mutations (e.g. DNA damage). Consider an immortal cell lineage. As this lineage proceeds through time the number of mutations may accumulate to a point where cellular function becomes detrimental to the organism (e.g. cancer), therefore it may be important for cells to die via apoptosis.
(3) ‘… Having been born to an older father could signal that an individual is likely to grow up in a social and ecological context within which mortality rates are low and reproduction is likely to occur later in life, thus placing more of a premium on a durable long-lived body….’
This is a really interesting point which links nicely to a study published in 2010, again in PNAS, which suggested that the upper and lower reproductive age limits in women were decreasing and increasing respectively. In a society where couples form primarily in an age-matched fashion, this is an important trend to ensure reproductive compatibility.
(4) '...We speculate that an effect of the age of paternal ancestors on TL could allow increases in life expectancy under demographic conditions of low mortality and delayed repro- duction, when investment in a more durable and long-lived body is likely to reap higher fitness returns.'
Here a couple of really interesting evolutionary questions arise. Think firstly of the necessary conditions which allow male individuals to offset reproduction until later in life.
In a population where the tendency to reproduce begins roughly at reproductive age, it can be assumed that all things being equal, any male who delays reproduction will be at an immediate disadvantage in terms of lifetime reproductive success (LRS) derived from fecundity (number of offspring). On the other hand, if this delay in reproduction conveys some selective advantage to a males offspring (as suggested in point 2), then his LRS in higher as a result of increased offspring survival.
In humans, the decision to offset reproduction may be a cognitive one in a socio-economic sense and so is not likely to be an evolved trait but rather a by-product of culture.
It is interesting to speculate that if TL is associated with lifespan and lifespan may affect when an individual chooses to reproduce, then this seemingly cultural trend could result in a true evolutionary shift in reproductive behaviour in humans.
Uncle Mick's HCGC
However, at the end of the chromosome the enzyme primase (which is responsible for the production of the short RNA primers found along the length of the lagging strand) does not have any downstream sequence which can be used as a substrate for subsequent primer synthesis. This leads to the degradation of the RNA portion of the Okazaki fragment without subsequent replacement with DNA. This leaves us with a small portion at the end of the chromosome which has not been replicated. Thus, with each round of cell replication, the ends of linear chromosomes get progressively shorter. Telomeres at the ends of our chromosomes, act as a buffer to the end replication problem by ensuring that non-coding repetitive sequence is lost rather than important DNA associated with gene function.