Maternal care modifies gene regulating key neurotransmitter

Physorg reports new research that emphasizes again the crucial epigenetic effects of maternal care of lack of it.

Researchers bred two different clades of rats, ones affective with their offspring and the others extremely detached. The offspring of the latter experimented an epigenetic modification obstructing the expression of the GAD1 gene, which regulates the key neurotransmitter GABA. 

GABA helps to regulate emotions and people with schizophrenia may have GABA deficits. Similarly the rats raised by the detached mothers also had low GABA production. 

Inversely, the rats raised by cuddly mothers showed high expression of GAD1. 

Rodents are genetically very close to primates and hence a very good model for our own biology even within the restricted spectrum of placental mammals. 

The research is attributed to Tie-Yuan Zhang to be published in September 29 in The Journal of Neuroscience.

Hyenas another european mammal extinct at the end of the last ice age

Spanish researchers have published a new paper on the extinction of spotted hyenas (Crocuta crocuta, the same species dominant in Africa) in Europe and Asia. Apparently hyenas lived without much trouble in the Mediterranean areas of Eurasia until c. 10,000 years ago, when they became extinct. This is also the time of the end of the last Ice Age.

Lead researcher Sara Varela says that climate change in the past was not directly responsible for the extinction of the spotted hyena in southern Europe, but it was a factor in its disappearance.

Source: Science Daily, illustration from Wikipedia.

Ref. Sara Varela et al., Were the Late Pleistocene climatic changes responsible for the disappearance of the European spotted hyena populations? Hindcasting a species geographic distribution across time. Quaternary Science Reviews 2010. Pay per view.

Signs of positive selection favoring disease risk genes

It is very much counterintuitive but that is what Stanford University researchers conclude after looking at the evidence.

Erik Corona et al., Extreme Evolutionary Disparities Seen in Positive Selection across Seven Complex Diseases. PLoS ONE 2010. Open access.

Abstract

Positive selection is known to occur when the environment that an organism inhabits is suddenly altered, as is the case across recent human history. Genome-wide association studies (GWASs) have successfully illuminated disease-associated variation. However, whether human evolution is heading towards or away from disease susceptibility in general remains an open question. The genetic-basis of common complex disease may partially be caused by positive selection events, which simultaneously increased fitness and susceptibility to disease. We analyze seven diseases studied by the Wellcome Trust Case Control Consortium to compare evidence for selection at every locus associated with disease. We take a large set of the most strongly associated SNPs in each GWA study in order to capture more hidden associations at the cost of introducing false positives into our analysis. We then search for signs of positive selection in this inclusive set of SNPs. There are striking differences between the seven studied diseases. We find alleles increasing susceptibility to Type 1 Diabetes (T1D), Rheumatoid Arthritis (RA), and Crohn's Disease CD) underwent recent positive selection. There is more selection in alleles increasing, rather than decreasing, susceptibility to T1D. In the 80 SNPs most associated with T1D (p-value less than 7.01×10⁻⁵) showing strong signs of positive selection, 58 alleles associated with disease susceptibility show signs of positive selection, while only 22 associated with disease protection show signs of positive selection. Alleles increasing susceptibility to RA are under selection as well. In contrast, selection in SNPs associated with CD favors protective alleles. These results inform the current understanding of disease etiology, shed light on potential benefits associated with the genetic-basis of disease, and aid in the efforts to identify causal genetic factors underlying complex disease.

Maybe the best understood case is that of rheumatoid arthritis, which, following the archaeological record, seems to have only manifested in west central Kentucky (USA) some 6500 years ago, slowly extending to other parts of North America (West Ohio some 1000 years ago) and then scattering worldwide after colonization. In contrast the alleles that favor the disease are much older everywhere and seem to work well against tuberculosis (TB). So it would be a clearly favorable allele (protecting against TB) until whatever (not yet known) pathogen or allergenic that triggers RA spread from the Ohio basin.

So now RA susceptibility alleles have become deleterious in those areas where TB is not anymore a problem but, until a few centuries ago, they were only being selected for, because there was no exogenous trigger for RA outside of the Ohio basin and instead they protected from tuberculosis.

A good example of how fitness value is therefore not absolute but contextual.

There are also some indications that T1D susceptibility alleles may be implied in defense against enteroviruses, which cause some pretty bad diseases such as poliomyelitis and meningitis.

Brain appears non-hierarchical, Internet-like

New research by the University of Southern California seems to confirm the non-hierarchical model of brain organization.

In the past it was common to believe that the brain was organized hierarchically, this preconception was challenged by the network hypothesis, which has been gradually growing in popularity. However neither model had much empirical support so far.

Now Richard H. Thompson and Larry W. Swanson have found that, at least for a particular region of the brain of rats, the reality is non-hierarchical but that of a complex network.

Richard H. Thompson and Larry W. Swanson, Hypothesis-driven structural connectivity analysis supports network over hierarchical model of brain architecture. PNAS 2010. Pay per view (depending on geography and time of access).

Press articles at Science Daily and BBC.

Corn syrup causes obesity

This is not "breaking news" because I read it some months ago but I totally forgot commenting about. It is anyhow something that has become part of my daily routine when in the supermarket: checking that whatever sweets I may buy do not have glucose syrup, which is the official term by which high-fructose corn syrup is marketed officially over here (EU normative, I presume), in spite of having more fructose than glucose.

From Science Daily (where you can read more details):

"When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they're becoming obese -- every single one, across the board. Even when rats are fed a high-fat diet, you don't see this; they don't all gain extra weight."

High fructose corn syrup is widespread in industrial foods, from sodas to cookies and nearly everything sweet because it is cheap (thanks to US subsidies to maize production), is sweeter than regular sugar (sucrose) and is easier to mix because of its liquid state. However there are still some brands that just use normal sugar.

Academic reference: Miriam E. Bocarsly et al., High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels. Pharmacology, Biochemistry and Behavior, 2010. Pay per view.

Hybridation pros and cons

An issue that has arisen more than once in discussions as of late, specially in relation with the recently discovered Neanderthal admixture in Eurasian Homo sapiens, is that of hybrid vigor or lack of it thereof. This is addressed at a new paper in PLoS Biology:

Ulises Rosas et al., Cryptic Variation between Species and the Basis of Hybrid Performance. PLoS Biology 2010. Open access.

Author summary:

A major conundrum in biology is why hybrids between species display two opposing features. On the one hand, hybrids are often more vigorous or productive than their parents, a phenomenon called hybrid vigor or hybrid superiority. On the other hand they often show reduced vigour and fertility, known as hybrid inferiority. Various theories have been proposed to account for these two aspects of hybrid performance, yet we still lack a coherent account of how these conflicting characteristics arise. To address this issue, we looked at the role that variation in gene expression between parental species may play. By measuring this variation and its effect on phenotype, we show that expression for specific genes may be free to vary during evolution within particular bounds. Although such variation may have little phenotypic effect when each locus is considered individually, the collective effect of variation across multiple genes may become highly significant. Using arguments from theoretical population genetics we show how these effects might lead to both hybrid superiority and inferiority, providing fresh insights into the age-old problem of hybrid performance.

A news article synthesizing the findings can be found at Science Daily:

The results show that hybrids might be expected to exhibit increased performance in basic traits such as growth. However, they also show that in the longer term, other traits such as those involved in sexual reproduction might be expected to perform less well, accounting for reduced fertility of hybrids.

Evolution of sperm

There is a fascinating new paper dealing with the origin and evolution of sperm production in animals.

Chirag Shah, M. J. W. VanGompel et al. Widespread Presence of Human BOULE Homologs among Animals and Conservation of Their Ancient Reproductive Function. PLoS Genetics 2010. Open access.


Author Summary

While sexual reproduction is widespread among animals, it remains enigmatic to what extent sexual reproduction is conserved and when sex-specific gametogenesis (spermatogenesis and oogenesis) originated in animals. Here we demonstrate the presence of the reproductive-specific protein Boule throughout bilaterally-symmetric animals (Bilateria) and the conservation of its male reproductive function in mice. Examination of Boule evolution in insect and mammalian lineages, representing the Protostome and Deuterostome clades of bilateral animals, failed to detect any evidence for accelerated evolution. Instead, purifying selection is the major force behind Boule evolution. Further investigation of Boule homologs among Deuterostome species revealed reproduction-specific expression, with a strong prevalence of testis-biased expression. We further determined the function of a deuterostomian Boule homolog by inactivating Boule in mice (a representative mammal, a class of Deuterostomes). Like its counterpart in Drosophila (a representative of the opposing Protostome clade), mouse Boule is also required only for male reproduction. Loss of mouse Boule prevents sperm production, resulting in a global arrest of spermatogenesis in remarkable similarity to that of Drosophila boule mutants. Our findings are consistent with a common origin for male gametogenesis among metazoans and reveal the high conservation of a reproduction-specific protein among bilaterian animals.


The authors argue that no positive selection is apparent in the Boule gene but only purifying selection.

... the low Ka/Ks [non-synonymous/synonymous mutation] ratio suggests that purifying selection was responsible for the strong functional constraint on the entire protein, making Boule an exception to the rapid evolution commonly seen in reproductive genes.

In other words: it is a key component of the reproductive system in males across animal species that cannot be easily altered without causing the collapse of the system.

They also tested for gene expression of the Boule gene in male and female reproductive systems across the Bilaterian taxon (animals with front and back sides), finding that this gene is only manifest in the male reproductive system, unlike DAZL, which manifests in both genders among the species it does exist (most vertebrates).

Another finding is that animals (mice in the experiment) with mutant Boule gene are perfectly normal except that they are infertile. They even have a normal mating behavior. The only apparent difference is in the testes, which are somewhat smaller. Similar effects were found in fruit flies.

However, inside the testes, the effect of the mutant Boule gene is dramatic, totally impeding spermatogenesis.


Further references:

• BOLL (Boule) gene at HUGO database (located in chromosome 2)
• DAZL gene at HUGO database (located in chromosome 3)
• DAZ1 (DAZ) gene at HUGO database (located in chromosome Y)
• DAZL gene at Wikipedia
• DAZ1 (DAZ) gene at Wikipedia
• Article at Science News

Inbreeding and fitness in mysid shrimps

There is an interesting new paper on a subject that often drives much discussion in this blog at least: how bad is inbreeding. The answer of course depends on several issues such as the intensity of inbreeding (not a mere true/false dichotomy) and the environmental pressure.

This paper deals with these matters in an experimental set with Americamysis bahia, a species of mysid shrimps.

Jeffrey E. Markert et al.,Population genetic diversity and fitness in multiple environments. BMC Evolutionary Biology, 2010. Open access.

The authors created a number of extremely inbred populations by

1. Taking a single pregnant female (presumably impregnated by a single male, as is typical in this species) from the main population (AMX) and removing it when the brood was released

2. Taking then one impregnated female from one of the resulting populations and another from a different one and placing them in the same tank until the brood was released.

3. Taking then one single impregnated female from the population resulting from step 2.

Overall it means that the hyper-inbred brood at the start of the experiment, described as 1X, had went through a narrow 2-4-2 bottleneck, being the equivalent to having 2.4 founders.

Populations of the type 2X, 6X and 8X were generated by mixing the respective number of 1X inbred populations, so they represent lesser degrees of inbreeding each.

By the end of the experiment, after 40 weeks, these were some of the results (more tables, graphs and explanations in the paper):



Figure 1 - Population fitness, estimated with Median Population Size (A), Last Census size (B), and Reproductive Index (C) [not shown here].
Paired box plots define the median and middle two quantiles in stressful (left) and permissive environments (right). Lower case letters unite groups that are not statistically distinguishable using post-hoc tests (Tukey’s HSD) at α = 0.05.

We can see that extremely inbred populations performed badly, specially in stressful environments (low salinity) but that not so extremely inbred ones performed reasonably well, specially in permissive (normal) environments.

While the results should not be strictly extrapolable to other species, we can reasonably conclude that a very low number of effective population founders (5 or so) seriously hampers survivability, specially in challenging environments, where essentially means a death sentence. However a not so tiny number of founders (25-30) can do quite well, in particular if the environment is favorable.

Sleep is brain's lunch time

There has always been a lot of discussion on why do we sleep. Now Boston researchers have found that it's when neurones get most of their food, showing very high levels of adenosine triphosphate (ATP), dubbed the "cell currency" of energy transfer, up to 3-4 times the normal levels.

When the experiment's rats had their sleep delayed by several hours this peak of ATP did not happen.

The neurones show in sleep period this high level of activity but brain's activity overall drops down. So I understand that their activity is selfish and relatively isolate unlike that of wake time, when they are working hard for the whole system to function properly.

Source: Science Daily.

I wonder: if sleep is neurones' lunch time, does that mean that dreams are their play time?

Folate and not cancer caused dark skin and the ability to tan

It is well known that depigmentation in humans was caused because of the need of vitamin D generation at the skin, but what was not so clear was why pigmentation, dark skin (conventionally called black, though it's actually brown in most cases) first evolved.

Researchers from Pennsylvania State University have now concluded that skin cancer, which is a quite weak selective pressure, is not the main reason for dark skin but the protection of folate (folic acid, vitamin B9) from being destroyed by the ultraviolet radiation.

Much like vitamin D deficiency can cause major problems in newborns, folate deficiency also does, causing neural tube defects, anemia, low birth weight and premature births. Additionally, it also affects, although less severely, adults, causing weakness, depression, weight loss, headaches and behavioral disorders.

Nina G. Jablonski and George Chaplin, Human skin pigmentation as an adaptation to UV radiation. PNAS 2010. Freely accessible (it seems).

Also discussed at Science Daily.

Breaking the seals of Life

The future is today. And that does not only applies to economics, Keynesian or purely Liberal, but also to technology, obviously.

But this technology is a bit too daunting, I fear. Making life out of four bottles of chemicals (sic) really hits hard on our sense of life, existence and even triggers instincts of self-preservation, an imprecise but deep fear.

The sensation is that a cosmic seal has been broken, that this door should never have been opened.

But of course rationality steps in and reminds that after all it is something that would have happened sooner than later. That this is what intelligence and knowledge carry with them. That Nature has been doing exactly that forever and that therefore it can be considered a precious gift from our mother: the ability to manipulate her very matrix.

The fear is after all one of acknowledging that the child, Humankind, is not mature enough for such a power, that it will most probably misuse it, causing much grief and maybe self-destruction.

But that's how things are. We don't get gifts from Nature anymore, we open our path quite ruthlessly through her secrets and guess that's alright for her, as long as it guarantees our survival... and if it does not, this other extinction, ours, will only make Mother Nature stronger in the long run anyhow.

The case, you may know by now, is that US researchers have managed to create bacterial DNA from scratch, insert it into a DNA depleted cell and get it to live and reproduce. They have created life out from scratch.

The same team, J. Craig Venter and his Institute managed to create a virus from scratch in 2003 and had already synthesized the bacterial genome from mere computer programs and chemicals in 2008 but then they failed to get it to work.

Considering the speed of research of this biotechnology, I can estimate that full human beings may be ready by 2050. Let's see: amoebas by 2017, simple multicellular beings (coral or fungus) by 2024, simple plants and animals by 2031, complex animals by 2038, humans by 2045.

What then? I can imagine the likes of Monsanto patenting brand new species of plants in few decades, animals soon later and then even, who knows?, artificial humanoids to serve as slaves or whatever.

Scary? Pretty much, I'd say.

More details on this shocking advance at:

· J. Craig Venter Institute
· The Guardian
· Science Daily

... and probably in most of your usual news sites.

Interfertile seal species retain different gene pools in spite of hybridation

This is probably a paper of interest for all those surprised or otherwise intrigued by the gene flow now detected between H. neanderthalensis and H. sapiens.

Melanie L. Lancaster et al. Two behavioural traits promote fine-scale species segregation and moderate hybridisation in a recovering sympatric fur seal population. BMC Evolutionary Biology 2010. Open access.

The two fur seal species share the same reproductive spot at Macquarie island in New Zealand (and two other sites) and they do engage in fact in rather high interbreeding. However the two species remain neatly separated because of habitat preferences (colder/warmer waters, pebble/boulder beaches) and maybe also proposed fitness costs for the hybrid offspring.

Some experts' opinions on the Neanderthal genome's implications

From Quo magazine (in Spanish). Translated some sentences here:

J.L. Arsuaga, co-Director of Atapuerca archaeological site: These are only some some results and we will have to wait. It is a contribution in some humans of just some 2%, what would not be really relevant.

C. Lalueza Fox, member of the research team of El Sidrón cave: This year we will see published the Thousand Genomes' Project, that aims to sequence a thousand human genomes, and will be interesting to see if the percentage of Neanderthal genes is kept, in which frequency, in which populations.

Jordi Agustí, member of the research team of Dmanisi site: It does not fundamentally invalidates what was believed so far: that they were different or almost different species.

E. Baquedano, member of the research team of Pinilla del Valle site: We will have to admit that Humans and Neanderthals belong to a single species even if they are distinct subspecies.

In the same magazine but a separate interview, anthropologist Erik Trinkaus, defends his theory on admixture in Europe some 40,000 years ago only and is disdainful of the use of aDNA and the comparison of a "pathetic" sample of just 3 Neanderthal individuals with just "five modern humans" (sic, actually it's five modern human populations comprising 12 individuals). He refers us to his 2007 anatomical paper.

Big brains not always better

At least in birds.

That's what Catalan researchers (in association with British and Canadian ones) have found among passeriformes: that migratory species have systematically smaller brains than resident ones. This seems to be caused because big brains with high exploratory behavior (pretty similar to our concept of intelligence) could be even dangerous for species that change space so often.

In the words of lead researcher, Daniel Sol:

For birds that travel a lot, exploring their surroundings produces more costs than benefits since the information which is useful in one place is not necessarily so in another. It also exposes them to more dangers. For these reasons we believe that for these species, their innate behaviour can be more useful than learned behaviour.

I find this association of brain size with what I'd call curiosity, intelligence, for what else is the ability to study your surroundings to exploit them optimally and maybe even creatively manipulate them, as do some birds such as crows.

More information at:

• D. Sol et al, Evolutionary Divergence in Brain Size between Migratory and Resident Birds. PLoS ONE 2010. Open access.
• Science Daily.

Genetics and biology: rather 'soft' sciences

That's what I gather from: D. Fanelli, “Positive” Results Increase Down the Hierarchy of the Sciences. PLoS ONE 2010. Open access.

It's an interesting research on the reality of the generally accepted hierarchy of the sciences between harder and softer ones. Fanelli measured, among other factors, the number of positive results reported when testing a hypothesis, which broadly are likely to be more the less rigorous a science is.

However applied sciences tend to break this rule, reporting in general more positive results and with little differences for the "hard" and "soft" sciences (see fig. 2).

So, once we remove the applied sciences (labelled as "a") from the above graph, it seems pretty obvious that some biological sciences (immunology, MB and genetics, biology, medicine and pharmacology) seem to have as much procedural bias or even "cheating" as the social sciences.

Vanity, procedural sloopinness and lack of rigor are likely to exist to some extent in these disciplines. The difference is of course one of degree (see fig. 3) but from c. 70% positive results to c. 90% there is a clear difference that probably means almost 25-30% of undeserved complacency for the worst scoring disciplines (the one mendtioned above).

It is also noticeable that highly regarded Psychiatry/Psychology scores a lot worse than the general Social Sciences. While the often criticized Ecology scores very well instead.

In any case one thing is clear: the expression "it's not rocket science" has all validity, as Space Science is the one with the best results.

Major breakthrough in differentiating between form and function coding genes

Researchers from Taiwan and the USA have been able to differentiate between some 900 morphogenes and a similar number of physiogenes (out of more than five thousand tested) in genetically modified mice. In the words of co-researcher Jianzhi Zhang:

We found very large differences." Morphogenes were more likely to carry instructions for transcription -- the step that determines whether a gene should be turned on and how much gene product should be manufactured. Physiogenes were more likely to be blueprints for enzymes, receptors, transporters and ion channels (molecules that control the flow of ions across cell membranes).

The finding also seems to seriously challenge some hypothesis that suggested that genes caused both types of effects simultaneously.

The researchers also compared these genes in tissue from different species and found more differences in morphogenes than physiogenes, what means that form evolves effectively faster than function.

Source: Science Daily.

Ref. Ben Yang-Liao et al., Contrasting genetic paths to morphological and physiological evolution. PNAS 2010. (Pay per view depending on world region, should be open access everywhere in six months).

Origin of small dogs in West Asia

New genetic research suggests that the alleles causing small size in certain dogs may have evolved early in the process of domestication and be derived from the wolf of West Asia (Canis lupus pallipes), of smaller size and tamer behavior than its more common relative Canis lupus lupus.

Melyssa M. Gray et al., The IGF1 small dog haplotype is derived from Middle Eastern grey wolves. BMC Biology, 2010.

See also the commentary by C.A. Driscoll and B. Macdonald: Top dogs: wolf domestication and wealth. Journal of Biology, 2010, arguing for a true origin of the dog in West Asian Mesolithic and later introgression of large size genes from the common wolf.

How to get life from the primordial ooze

While the potential for the basic bricks of life to form was demonstrated early in the history of modern science, how could these organic molecules get together to become the long chains of RNA or DNA, and hence life, has remained a mystery.

The problem is that oligonucleotides react and don't bind together under normal conditions. However researchers from the Georgia Institute of Technology have found now that certain "midwife" molecules, known more technically as "intercalators" cause such binding, creating longer polymers, RNA or DNA, the kernel of life.

Hence one of the main problems of paleo-biology seems to have been solved.

Read more at Science Daily.

Polyamory prevents extinction

... in fruit flies at least.

Tom A.R. Price et al, Polyandry Prevents Extinction. Current Biology, 2010.

There's also an article at Science Daily.

There seems to be a sex-ratio distortion (SR) X chromosome among some males that kills all the Y chromosome sperm before it can fertilize the egg, hence tending to produce an all-female offspring. By mating with various males, females prevent that this SR chromosome can become dominant up to the point of becoming a female-only population bound to extinction.

From the paper:

SR is a naturally occurring X chromosome meiotic driver that kills the Y chromosome-bearing sperm of male carriers [9,17]. SR therefore results in all-female broods and is inherited by all of the offspring of females that mate with male carriers [18,19]. This transmission advantage allows SR to spread through populations. However, the loss of half of the sperm produced by SR carriers makes them poor sperm competitors, with SR males...

Fruit fly populations in which females were forced by researchers (who acted as some sort of religious police, like in Saudi Arabia) to mate only with one male each, ended up after just 15 generations too crowded with this SR chromosome and five out of twelve (almost 50%) went extinct. Instead the control populations where free mating was allowed, remained healthy and kept the SR chromosome under control.

This seems to have implications beyond Drosophila pseudoobscura, the species used in this research, because both the "selfish" SR chromosome and the existence of promiscuity seem to be widespread through the animal kingdom.

It is quite curious how selfish genes, or in this case full chromosomes, do seem to exist but nevertheless they are not advantageous to their carriers. It is also curious how a mere drive in favor of diversity, such as promiscuity, helps to keep such genetic nuisances under control.

Molecular clock speculation obscuring the real Jurassic origin of primates

Again reality and reason clash frontally with the molecular clock hypothesis (or at least the most common interpretations of it).

If we'd have to follow the molecular clock speculations, so fashionable these days, we'd have to have sailor monkeys, which would have crossed oceans to get into America already in the Eocene, when the Atlantic Ocean was already huge. Such a colossal feat is plainly impossible, even for humans before just some centuries ago, but the fanatics of the molecular clock religion have argued for transoceanic rafting and hypothetical "island hopping" en masse.

Non-human primate range.

Common Sense shakes its head in disbelief, Folly laughs delighted at the naivety of even some of the supposedly most brilliant human minds.

Luckily Reason still has good cards to play in this surrealistic meta-game of honest facts versus trickster blind faith. The card that Reason plays now reads:

Michael Heads, Evolution and biogeography of primates: a new model based on molecular phylogenetics, vicariance and plate tectonics. Zoologica Scripta 2010.

Abstract:

The ages of the oldest fossils suggest an origin for primates in the Paleocene (∼56 Ma). Fossil-calibrated molecular clock dates give Cretaceous dates (∼80–116 Ma). Both these estimates are minimum dates although they are often 'transmogrified' and treated as maximum or absolute dates. Oldest fossils can underestimate ages by tens of millions of years and instead of calibrating the time-course of evolution with a scanty fossil record, the geographical boundaries of the main molecular clades of primates are calibrated here with radiometrically dated tectonic events. This indicates that primates originated when a globally widespread ancestor (early Archonta) differentiated into a northern group (Plesiadapiformes, extinct), a southern group (Primates), and two south-east Asian groups (Dermoptera and Scandentia). The division occurred with the breakup of Pangea in the Early Jurassic and the opening of the central Atlantic (∼185 Ma). Within primates, the strepsirrhines and haplorhines diverged with volcanism and buckling on the Lebombo Monocline, a volcanic rifted margin in south-east Africa (Early Jurassic, ∼180 Ma). Within strepsirrhines, lorises and galagos (Africa and Asia) and lemurs (Madagascar) diverged with the formation of the Mozambique Channel (Middle Jurassic, ∼160 Ma). Within haplorhines, Old World monkeys and New World monkeys diverged with the opening of the Atlantic (Early Cretaceous, ∼130 Ma). The main aspects of primate distribution are interpreted as the result of plate tectonics, phylogeny and vicariance, with some subsequent range expansion leading to secondary overlap. Long-distance, trans-oceanic dispersal events are not necessary. The primate ancestral complex was already widespread globally when sea-floor spreading, strike-slip rifting and orogeny fractured and deformed distributions through the Jurassic and Cretaceous, leading to the origin of the modern clades. The model suggests that the topology of the phylogenetic tree reflects a sequence of differentiation in a widespread ancestor rather than a series of dispersal events.

The paper is behind paywall but you can read a synthesis at Science Daily.

The molecular clock, if it still makes any sense at all, is certainly much slower. Primates migrated to South America in the Jurassic, when it was still part of Gondwanaland.