Here's the entire J.E.T Channell paper for anyone interested:
cnr.it
The most important bit:
4. Neanderthal extinction
The extinction of Neanderthal represents one of the great puzzles of human evolution.
Neanderthal and anatomically modern humans (AMHs) cohabited Western Europe for
~2-5 kyr, prior to ~39 ka, supporting the contention that competition may have
contributed to the demise of Neanderthal (Higham et al., 2014). Brief cold and dry
conditions in Europe associated with Heinrich Stadial (HS) 4 were proposed as an
additional likely stressor on Neanderthal (Sepulchre et al., 2007). Analyses of
Campanian Ignimbrite (CI) cryptotephra from archaeological sites in Greece and
elsewhere in Eastern Europe and Libya indicated that the CI eruption occurred early in
a dry period associated with HS4, postdated the end of the Middle Paleolithic and the
Mousterian tool industry, and hence postdated the demise of Neanderthal (Lowe et al.,
2012). In Black Sea sediment cores, CI tephra overlie, and therefore postdate, the
Laschamp excursion (Nowaczyk et al, 2012).
The extinction of Neanderthal and the demise of the Mousterian tool industry (Fig. 3)
can be placed at 41,030–39,260 calibrated years before present (41-39 ka) with 95.4%
probability (Higham et al., 2014). Cooper et al. (2015) estimated the extinction of
Neanderthal at 41,227 calibrated years before present (BP) with a standard deviation of
219 years, and 39,528-41,013 calibrated years BP using the GRIWM method (Fig. 2).
Mousterian ages outside this range have been recorded at several locations in southern
Iberia including Gorham’s Cave in Gibraltar (Finlayson et al., 2006; Tzedakis et al.,
2007), but these ages should now be disregarded according to Higham et al. (2014).
Recent findings cast doubt on the existence of Neanderthal after ~39 ka, and lead to a
closer correspondence of the demise of Neanderthals with the Laschamp magnetic
excursion and the associated brief interval of very low geomagnetic field intensity
centered at ~41 ka (Laj et al., 2014). It is important to note that the IntCal13
radiocarbon calibration (Reimer et al., 2013) may be offset to older ages by ~1 kyr in
the vicinity of the Laschamp excursion, relative to ice-core chronologies (Muscheler et
al., 2014).
Valet & Valladas (2010) proposed that low magnetic field strength in the
Laschamp/Mono Lake excursion interval (40-33 ka) was an important factor in
Neanderthal demise. Why anatomically modern humans (AMHs) were not similarly
affected has remained an open question considering that the two populations shared
habitats for 2600-5400 years (Higham et al. 2014) or >5 kyr (Lowe et al., 2012). There
is no evidence for differences in skin pigmentation between European AMHs and
Neanderthals, and at least a fraction of Neanderthals apparently had the same pale skin
and/or red hair observed in some modern humans (Lalueza-Fox et al., 2007). Natural
skin pigmentation in humans mitigates the harmful effects of UVR but its advantage is
offset by the importance of sunlight for vitamin D3 synthesis. The skin protection factor
(SPF) of “red ochre” (hematitic iron oxides) is traditionally utilized by some African
tribes (Rifkin et al., 2015) and has been used since at least the last interglacial (~120
ka) based on ochre coatings on strung beads and residues on storage shells from Africa
(Hodgskiss & Wadley, 2017), SE Spain (Hoffmann et al., 2018) and Levantine
Mousterian sites (Bar-Yosef Mayer et al., 2009). The mystery of AMH survival at the
time of Neanderthal demise may have been resolved by the discovery of differences in
amino acid substitution in an intracellular chemosensor (the aryl hydrocarbon receptor,
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532 AhR) for AMHs and for Neanderthals and other primates (Hubbard et al., 2016).
5. The role of the aryl hydrocarbon receptor (AhR)
Defense mechanisms against UVR include the production of quenching agents and anti
oxidant enzymes that neutralize reactive oxygen species (ROS) produced by UVR. The
ROS modulation is controlled by the AhR intracellular chemosensor that plays a key role
in the evolutionary response to UVR. Experimental results indicate an adaptive
response of mitochondria to varying ROS levels under a phenomenon called
mitohormesis (Becker et al., 2016).
The primary role of AhR is to regulate the transcription of genes mediating responses to
the biochemical and toxic effects of dioxins, polyaromatic hydrocarbons, and related
compounds (Abel & Haarmann-Stemmann, 2010). AhR is expressed in all skin cells and
can be generated by UVR through an endogenous ligand formed in situ from an amino
acid called tryptophan (Esser et al. 2009). UVR and the more harmful UVB (wavelength
290-320 nm) is absorbed by free tryptophan in the cytosol of epidermal cells, and AhR
plays a key role in translocating UVR stress response to the nucleus (Wei et al., 1999;
Fritsche et al., 2007; Tigges et al., 2014). Exposure to UVR, particularly UVB, generates
highly mutagenic DNA photoproducts. The process initiates apoptosis and involves
damage to nuclear DNA accompanied by mitochondrial dysfunction (Frauenstein et al.,
2013). There is a general consensus that the AhR of modern humans is implicated in
DNA repair (Schreck et al., 2009; Dittmann et al., 2016), tumor suppression (Fan et al.,
2010; Yu et al., 2017), epidermal barrier function (Noakes 2015), skin tanning response,
and melanocyte homeostasis (Luecke et al., 2010; Jux et al., 2011). Phylogenetic analysis
suggested that the ability of vertebrate AhR to sense xenobiotics was acquired at a late
stage of evolution, implying that the driving force for evolutionary conservation of AhR
lies not only in its role in xenobiotic metabolism but also in normal cell development
(Hao & Whitelaw, 2013; Hahn et al., 2017).
Hubbard et al. (2016) showed that the AhR variant in modern humans contains Val381
residue in the ligand-binding domain, while the AhR of Neanderthals, and a Denisovan
individual, as well as non-human primates and other vertebrates (rodents) encode the
ancestral Ala381 variant. The Val381 variant is fixed in the genome of all modern
humans as well as in the genome of the oldest (45 ka) AMH individual sequenced to
date (Fu et al., 2014). Hubbard et al.(2016) suggested that the unique modification of
AhR in AMHs led to significant competitive advantage over their Neanderthal neighbors,
due to decreased sensitivity in AMHs to toxins associated with fire-smoke, the effects of
which may have been exacerbated by troglodytic lifestyles.
Our focus here is on AhR involvement in the regulation of the skin responses to UVR,
especially to harmful UVB radiation, and its modulation of the immune system (Rannug
& Fritsche, 2006; Agostinis et al., 2007; Esser et al., 2013). UVB induces two signaling
routes in mammalian cells: first, UVB is absorbed by nuclear DNA that results in
generation of DNA photoproducts, and second, UVB activates cell-surface receptors
(Merk et al., 2004). AhR plays an important role in skin integrity and immunity. AhR
activation leads to transcriptional gene activation, and is involved in the cutaneous
stress response to UVR (Agostinis et al., 2007; Dittmann et al., 2016; Schwarz, 2005;
Navid et al., 2013) and alterations of gene expression (Dugo et al., 2012). Activation of
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AhR by UVB leads to signaling both to the nucleus and to cell membranes (Fritsche et al.,
2007). The findings show that UVB irradiation affects cell surface receptors with
subsequent activation of mitogen-activated protein kinases that in turn affect DNA in
the nucleus. |
