In addition, the camera eye of vertebrates including mammals, cephalopods including squid and octopus, and cnidarians including jellyfish is another example of convergent evolution. Homology refers to the existence of shared ancestry between a pair of structures or genes in different taxa while convergent evolution refers to the independent evolution of similar features in species of different periods in the timeline.
Homology is the evolution of similar structures in species evolved from a recent common ancestor whereas convergent evolution is the independent evolution of similar structures in unrelated organisms. Homology is a type of divergent evolution while convergent evolution is the opposite form of divergent evolution. Homology develops homologous structures while convergent evolution develops analogous structures.
Homologous structures have similar structures but, different functions while analogous structures have different originations of structures but, similar functions. Homology has a high degree of genetic similarity while convergent evolution does not develop any genetic similarity. Homology occurs as a result of evolutionary relationships while convergent evolution occurs as an adaptation in response to the changes in the environment. Homology is the development of similar anatomical structures species with common ancestry.
Significantly, although these structures are homologous structures, which are similar in anatomy, they have different functions. However, they exhibit a significant level of genetic similarity.
In contrast, convergent evolution is the independent development of similar anatomical structures in unrelated species. See text for in depth description. Large body sizes and significant longevities evolved multiple times. The numbers inside the arrows indicate the fold difference in maximum longevity and adult weight from the smaller to the higher value. The Phylogenetic tree was built following phylogenetic information in Gomes et al. Maximum longevity and adult weight were taken from the AnAge database Tacutu et al.
Time scale is given only as a reference and it is not meant to be accurate My, millions of years ago. Support of this theory comes in part from the fact that several human premature aging syndromes are characterized by defects in single genes coding either for DNA repair proteins or for lamin A, a protein primarily involved in nuclear architecture with the capacity to influence genomic stability.
Based on the DNA damage accumulation theory, we might suggest that convergent evolution could be involved in increasing genomic stability in long-lived species. Large body size and long life span have evolved multiple times in independent branches of the phylogenetic tree of life.
Omitting for a moment the DNA damage theory of aging, we can hypothesize that convergent evolution in cellular machineries could also play a role in the evolution of large body masses. It is reasonable to expect, in fact, that large species, having more cells, would be at higher risk of cancer if, with the increase in size, genomic stability mechanisms are not concurrently improved Peto With these considerations in mind, we have searched for cellular characteristics that have the potential to provide longevity assurance across mammalian species that vary in adult size and in longevity.
To date, our laboratories, have analyzed: 1 the capacity of somatic tissue for extensive proliferation while maintaining a normal diploid chromosome content, 2 telomere length and 3 the capacity to detect DNA damage at the molecular level. In this review, the focus is this body of work and work strictly related to these subjects from other authors.
For this reason, we ask forgiveness if this review is not comprehensive of all relevant literature. Hayflick and Moorhead demonstrated that somatic cells have a limit in the number of cell divisions they can achieve Hayflick and Moorhead , contradicting the preexisting paradigm according to which cells isolated from the body have an unlimited replicative capacity Carrel Hayflick also suggested that this limit is a general characteristic of all normal diploid cells and that unlimited replicative capacity is a characteristic of cancer cells abnormal cells.
Another suggestion was that this limited replicative capacity represents aging at the cellular level. Additionally this idea has two obvious and testable implications: the first is that cells from younger individual are expected to be able to accomplish more cell divisions than cells from old individuals; the second is that cells from long-lived species are expected to be able to accomplish more cell divisions than cells from short-lived species Fig.
Two expectations from the hypothesis that the maximum number of cellular divisions in vitro relates to species longevity. Regarding the first implication, much research has been performed, almost exclusively, evaluating replicative capacity in culture because of the scarcity of reliable techniques that will allow tracking replicative capacity of cells in vivo. This literature has been revised in one chapter of the above mentioned book Lorenzini and Maier In this assay, the authors concluded that the first implication is not supported, at least for skin fibroblasts that are the cell type mainly used for this kind of studies.
For the sake of completeness, we should mention that in vitro colony forming ability could be related somehow to donor age also reviewed in Lorenzini and Maier A relationship that could depend from a decrease in the speed of doubling with increasing donor age. Decrease that has been observed in human skin fibroblasts Kalfalah et al.
Regarding the relationship between replicative capacity measured as number of cell doublings and species longevity less research is available. Stanley and coworkers, measuring replicative capacity of ten cell strains each from a different mammalian species, concluded that there is not relationship between replicative capacity and longevity Stanley et al.
A larger study by Lorenzini et al. In other words, the cells from large species are the ones capable of sustaining multiple rounds of division while preserving a normal karyotype. Moreover, they are able to sustain proliferation to a greater extent than cells from long-lived but small sized species.
It is known that oxygen negatively affect in vitro replicative life span Balin et al. Accepting this criticism, we may reformulate the above finding stating that replicative capacity under stressful ambient oxygen conditions correlate primarily with species adult body size than to longevity. Gillooly et al. The observations that telomere loss is minimal in skin of old donors [ Krunic et al. Conversely, the cells derived from the biopsies of taller nonagenarians had less residual replicative capacity compared with the cells derived from the shorter ones Maier et al.
In other words, the requirement to cover the larger surface of a taller body during development leave the cells in the adult with less residual proliferative capacity. If the number of potential cell divisions was related to longevity, one would predict that taller individuals the one with less residual replicative capacity should be the short-lived ones. This appears not to be the case; see for example, a recent large meta-analysis showing a positive association between stature and longevity NCD Risk Factor Collaboration As already mentioned, body mass and longevity are loosely and positively linked among species.
The simplest explanation for this relationship is that even with very fast proliferation rates, very large bodies will require longer developmental time than small bodies since every organism starts from a single cell. The complex issue regarding the intraspecies relationship between body size and longevity, marginally addressed above, is not the focus of this review and is discussed in more depth elsewhere Bartke ; Lorenzini ; Samaras The spindle assembly checkpoint blocks progression into telophase if the chromosomes are not correctly aligned at the mitotic spindle equator Musacchio and Salmon We have performed a small investigation on the efficiency of this checkpoint on six mammals using cultured fibroblasts and the results support our above stated view Lorenzini et al.
We have observed that the efficiency of this checkpoint is higher in large species, while species longevity does not appears as a key factor. Although this analysis suggests that an increased efficiency of the spindle assembly check point could be more important for evolving large body size than longevity, this does not exclude the possibility that aneuploidy may negatively affect life span as well.
Baker et al. Additional support of our hypothesis comes from a meta-analysis we have performed on the spontaneous in vivo frequencies of micronucleated erythrocytes. The spontaneous appearance of micronuclei in circulating erythrocytes is a sign of poor mitotic efficiency during erythropoiesis.
Collecting data from eight pre-existing studies we have found that the frequency of micronucleated erythrocytes correlates primarily with body mass rather than longevity Croco et al. We should note that this is a negative correlation. These data suggest that, although both large bodies and long-lived bodies require the production of a large number of erythrocytes by the bone marrow, size is the most important constraining factor requiring a more efficient cellular machinery for replicating the genome.
The capacity to detect molecular damage is a potential cellular determinant of longevity. Detecting the presence of damage is a necessary step in order to proceed with repair or, if the damage is irreparable, with other means of damage control, as the induction of cellular senescence or apoptosis.
Because of its hierarchical role, the most serious molecular damage is DNA damage. This is because NHEJ is active throughout the cell cycle, whereas HR is typically active only during the S and G2 phases, and the majority of cells in the adult body are in G0 Rothkamm et al.
Intraspecies observations support a role of NHEJ in cancer and aging. In humans, a decrease in DNA end-joining capacity is associated with an increase in breast cancer risk Bau et al.
Stamato and colleagues have developed a method to study the initial step of NHEJ: the recognition of double stranded DNA breaks or DNA ends by nuclear proteins, a property that is strictly ascribable to the Ku heterodimer Getts and Stamato This method consists of two steps. The first step is based on a competitive binding between a nuclear proteins extract, a 32 P labeled linear DNA probe and an excess of unlabeled circular plasmid DNA containing the same sequence of the linear DNA probe as competitor.
Since the circular plasmid is in large excess fold ratio competitor to probe , nuclear proteins with affinity for particular sequences, present in the probe, will bind the excess circular plasmid and only the protein with affinity for DNA-end will bind the labeled probe. The second step consist of an estimation of the amount of binding complexes by measuring the proportion of shifted probe on a southern blot Fig. DNA-end biding assay. The slowing down in the probe migration shift is evidence of the formation of complexes between DNA-ends and proteins.
Using this assay, Lorenzini et al. The results show a striking, positive relationship between DNA-end binding and species longevity Lorenzini et al. What makes this relationship interesting is the lack of a correlation between DNA-end binding activity and species adult body mass. Thus, the end-binding activity appears to be more closely related to longevity than other mechanisms of genomic surveillance. Both of these events can be assayed by immunofluorescence.
Since these markers of genomic damage can be measured with ease, they are largely used in basic science and their use could move to the clinic in the near future Somaiah et al. Kalfalah et al. Waaijer et al. At this regard, 53BP1 protein up-regulation was observed in human fibroblasts isolated from long living subjects centenarians compared to young and old donors, in absence of any changes of the phosphorylated active form of 53BP1 Lattanzi et al.
Notably, in cells from centenarians exposed to oxidative stress a higher level of phosphoactiveBP1 nuclear foci accumulation and their rapid clearance compared to younger controls was observed. The above described scenario in centenarian fibroblasts is reminiscent of literature data reporting a repression of HR repair in in vitro replicative senescence giving the way to the 53BP1 dependent mechanism Mao et al.
Notwithstanding this evidence, the up-regulation of NHEJ recombination pathway in centenarians represents a reshaping of the DNA damage response rather than a decline in the DNA repair capability Lattanzi et al.
At this regard, it is necessary to take into account that histone methylation status affects aging of adult stem cells in which DNA damage repair is a pivotal driver of tissue aging and dysfunction Pollina and Brunet Consequently, it is necessary to deepen our understanding of the role of 53BP1 in the different modalities of NHEJ see discussion and Ciccia and Elledge and more studies are needed to unravel the links between epigenetic regulation, genomic stability, NHEJ and human longevity.
We tested whether, even by this other mean to respond to genotoxic damage, long-lived species have more efficient cellular machineries. To this end, we have exposed skin fibroblasts derived from different mammals to the same concentration of two genotoxic agents etoposide and neocarzinostatin.
We found that long lived species display higher abundance of DNA damage nuclear foci Fink et al. Since these markers are used to study the presence of DNA damage and a higher presence of these markers is usually interpreted as a higher presence of damage, we also evaluated DNA damage using direct assays such as the comet assay and the micronucleus assay.
The first assay measures DNA fragmentation while the second measures if a whole chromosome or a fragment has been separated from the rest of the genome during mitosis.
Our analysis has revealed that longer-lived species display both a lower level of DNA damage measured by these two direct assays relative to shorter—lived species, and a higher presence of DNA damage nuclear foci. These results suggest a lower level of damage coupled with an enhanced damage response. This is consistent with the DNA-end binding data. The variation, we have observed, in the ability to bind DNA-ends is extremely large: fold from mouse to human.
Thus the differential abundance could, in itself, explain the difference in DNA-end binding activity Lorenzini et al. The hypothesis that specific cellular functionalities, necessary to guarantee genomic stability, may be upregulated simply by increasing the abundance of key proteins it is a straightforward one. Sulak et al. This ensues in an increased expression of the oncosuppressor following genotoxic stressors and a consequent increase in apoptosis in comparison to phylogenetically closely related species hyrax, aardvark, and armadillo that are much smaller and have only one or two copies of TP With this knowledge in hand, we can see that the development of camera eyes in these lineages is not as improbable as we might have thought at first.
In all three cases, these lineages built a camera eye around a preexisting molecular system for detecting light. The camera eyes themselves might be convergent, but they are based on a deeper underlying homology that improved the odds that they would appear through successive modifications of an ancestral system.
Both groups use highly tuned echolocation for navigation and seeking prey in an environment where visual perception is limited or lacking altogether. The evidence that the development of echolocation in these two very divergent groups of mammals is due to convergent evolution is strong — no other mammals more closely related to either group has such an ability.
Cilia also change their length and vibratory properties in response to different auditory stimuli. The vibrations are used to change the flow of electrical charge in these cells, eventually leading to nervous system signals that the brain perceives as sound.
All mammals use a protein called prestin as part of the auditory system. What is interesting, however, is that in these groups the prestin protein has been independently shaped through natural selection to be tuned to high frequency ultrasonic sound more useful for echolocation.
In fact, in a phylogeny restricted to prestin sequences, bat prestins and toothed whale prestins appear to be the most closely related to each other — a finding wildly at odds with the species tree for bats and whales. Further examination, however, shows that these striking similarities are the result of convergent evolution, not a more recent shared ancestry. One common misconception I encounter about evolution is that it is predominantly a random process — one that is mainly influenced by chance events.
While we have already shown that evolution has a strongly non-random component natural selection , this discussion of convergent evolution further demonstrates that evolution is repeatable in certain important ways. When natural selection affects distantly-related groups in a similar fashion, we often observe similar outcomes. These similar outcomes are in many cases favored by prior history homology and arrived at through similar, but not identical paths demonstrating that contingency and chance are present as well.
Evolution is thus a balance of contingent events mutations and other chance events and emphatically non-contingent events selection, convergent evolution. Join us to receive the latest articles, podcasts, videos, and more, and help us show how science and faith work hand in hand.
If a gene has variation in a population undergoing speciation events, it is expected that some of the time it will assort with a pattern that does not match the species pattern Moths that are merely using a warning sound to advertise their toxicity emit signals in a pattern that does not produce interference with bat echolocation Does human genetic variation today provide evidence that we can trace our ancestry exclusively from a single couple?
Biology, philosophy and religion work together to help us to understand the world we live in and to better know God. Part Three in the Uniquely unique mini-series. We look to morality, language, and culture, and start to see that our species is quite an outlier. Author of "Thriving with Stone Age Minds," Justin Barrett responds to the reaction some people have to the idea of evolutionary psychology.
Part Two in the Uniquely unique mini-series. When we look for what makes humans unique on this planet, looking at our biology is an obvious first step. Birds of a feather One classic example of a homoplasy is powered flight in birds and some mammals i.
Homoplasy vs. Based on these data alone, the simplest most parsimonious phylogeny would be as follows:. The power of convergence Since homoplasies act as markers that flag repeated evolutionary events, looking for homoplasies in species trees is a useful way to test hypotheses about the reproducibility of evolution, or how often species converge on similar solutions.
There are numerous examples of repeated, independent innovations over evolutionary history, some of which we will examine in more detail in upcoming posts: Streamlined body shape: the streamlined body form of aquatic life such as fish, ichthyosaurs, whales, seals and diving birds e. Powered flight: in addition to birds and bats, powered flight also evolved independently in insects and pterodactyls. Echolocation: some mammals, such as bats and whales, have independently developed systems that allow them to locate food through detecting how sound that they generate echoes off structures and prey in their environment.
Camera eyes: the repeated evolution of camera eyes i. Camera eyes have independently evolved in cnidarians certain jellyfish , cephalopods such as squid and octopus and vertebrates birds, mammals.
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