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Bertolesi, G. E.

Publications and source records attributed to Bertolesi, G. E..

3 recordsLinked to original sources

Magnetosensitivity of amphibian morphological pigmentation is light- and eye-dependent and consistent with the radical pair mechanism

Weak magnetic fields influence a wide range of biological processes, yet the underlying mechanisms are poorly understood. The radical pair mechanism (RPM), which involves quantum spin dynamics, is a leading hypothesis. Here we show that weak magnetic fields modulate morphological pigmentation--specifically, the number of perioptic melanophores-- in Xenopus laevis tadpoles in a field-strength-dependent manner. The response is light- and eye-dependent. The observed field-strength dependence is quantitatively consistent with a radical pair model. These properties are reminiscent of the light-dependent magnetoreception that is thought to operate in migratory birds, and establish amphibian pigmentation as a tractable vertebrate system for the study of radical-pair quantum biology. Significance statementWhether weak magnetic fields can influence vertebrate physiology through quantum spin dynamics has been difficult to test in a living animal. We show that weak magnetic fields alter the number of perioptic melanophores in Xenopus laevis tadpoles through a light- and eye-dependent mechanism whose field-strength dependence is quantitatively consistent with a radical-pair mechanism. Amphibian pigmentation thus offers a genetically tractable vertebrate system in which radical-pair quantum biology can be tested against whole-organism physiology.

biophysics↗

Evolutionary Adaptations of TRPA1 Thermosensitivity and Skin Thermoregulation in Vertebrates

Altering skin color and reflectance is crucial for temperature regulation in poikilothermic vertebrates, while less so in homeotherms like birds and mammals, which evolved feathers, fur, and other insulation for endothermy. Heat-sensing in vertebrates relies primarily on Transient Receptor Potential (TRP) channels, with certain channels (TRPA1) shifting thermosensitivity over evolution and others retaining heat sensitivity (TRPV1). Exploration of a role for TRP channels in skin physiology has largely focused on human pigmentation and overlooked the evolution of different thermoregulatory structures in the integument of distinct vertebrates. For instance, colour/reflector pigment cells in ectotherms, fur and feathers in endotherms, hairless skin in hominids, and blubber in marine mammals. Therefore, we investigated whether a TRP channel mediates skin darkening induced by heat in the ectotherm Xenopus laevis and then explored the evolution of TRPA1 thermal sensitivity and its link with skin physiology. We find Trpa1 mediates heat-induced melanosome dispersion, darkening skin under warmer conditions. In contrast, TRPA1 is known to mediate cold sensation in rodents and UV-induced tanning in humans, leading us to investigate the co-evolution of TRPA1 and skin thermoregulation. Our findings reveal TRPA1 is a heat sensor in ectotherms with uncovered integuments. In mammals, we suggest TRPA1 was thermally insensitive in Euarchontoglires but became cold-sensitive in several rodent lineages. TRPA1 shows reduced selection pressure for thermosensitivity in aquatic mammals (manatees, whales) that depend on blubber for insulation as compared to their terrestrial relatives. These findings emphasize adaptive evolution of TRPA1 in vertebrates, linking thermal sensitivity to the evolution of skin physiology.

evolutionary biology↗

Interplay of Light, Melatonin, and Circadian Genes in Skin Pigmentation Regulation

HighlightsO_LICircadian pigmentation of tadpoles in vivo is mainly driven by melatonin C_LIO_LILight and melatonin differentially regulate proliferation C_LIO_LIMelatonin mimics the expression of circadian core genes in the dark phase C_LIO_LIDeregulation of the circadian rhythm inhibits melanin synthesis C_LI Circadian regulation of skin pigmentation is essential for thermoregulation, UV protection, and synchronization of skin cell renewal. This regulation involves both cell-autonomous photic responses and non-cell-autonomous hormonal control, particularly through melatonin produced in a light-sensitive manner. Photosensitive opsins, cryptochromes, and melatonin regulate circadian rhythms in skin pigment cells. We studied light/dark cycles and melatonin coordination in melanin synthesis and cell proliferation of Xenopus laevis melanophores. In vivo, tadpole pigmentation shows robust circadian regulation mainly hormone-driven, in that isolated melanophores respond strongly to melatonin but only slightly to light. Melanophore proliferation is faster in the dark and slower with melatonin compared to a 12/12 light/dark cycle. Expression of circadian core genes (clock, bmal1, per1, per2, per3, cry1, cry2, and cry4) in melatonin-treated cells during the light phase mimics dark phase expression. Individual Cry overexpression did not affect melanisation or cell proliferation, likely due to functional redundancy. Melanin synthesis was inhibited by circadian cycle deregulation through: a) pharmacological inhibition of Cry1 and Cry2 degradation with KL001, b) continuous light or dark conditions, and c) melatonin treatment. Our findings suggest that circadian cycle regulation, rather than proliferative capacity, alters melanisation of melanophores. SignificanceCircadian rhythms are a highly conserved phenomenon in nature. In vertebrates, the modification of skin pigmentation and epidermal cell renewal in response to the environmental light-dark cycle are crucial physiological adaptations that serve various purposes, including thermoregulation, reducing ultraviolet damage, and regulating skin stem cell proliferation. Our observations indicate that, in vivo, the circadian regulation of skin pigmentation is more influenced by cycling-melatonin levels than light/dark. The deregulation of the circadian cell cycle through various mechanisms all inhibited melanisation while cell proliferation was increased or reduced, suggesting that proliferation and melanisation are mechanistically dissociated responses. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=125 SRC="FIGDIR/small/604624v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@9787deorg.highwire.dtl.DTLVardef@59022corg.highwire.dtl.DTLVardef@19dd46eorg.highwire.dtl.DTLVardef@e58fec_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical AbstractC_FLOATNO C_FIG

physiology↗