The Greenland shark’s eye has become an unlikely archive of deep time.
Proteins sealed inside the eye lens helped researchers establish that this animal can live for centuries. Now the living tissue behind the lens is offering a second surprise: the visual system appears to remain intact and molecularly active for more than a human lifetime.
Researchers examining adult Greenland sharks estimated to be over 100 years old found no obvious retinal degeneration. The cells needed for dim-light vision were present, their genes were active, and the shark’s main visual pigment was tuned to the blue light that travels farthest through deep Arctic water.
The team also found strong expression of DNA-repair genes in the retina. Those genes may help maintain the eye across an extreme lifespan, although the study did not prove that they cause the preservation.
The result, published in Nature Communications, is more careful and more interesting than saying a centuries-old shark passed an eye test. No living animal was asked to identify a shape or follow a target. Instead, several independent measurements converged on a visual system that still appears capable of working.
The First Fleet comparison is plausible, not a birth certificate
The First Fleet reached Botany Bay on 18 January 1788 and settled at Sydney Cove eight days later. Could a Greenland shark alive in modern times really have been swimming then?
The answer is yes, within the large uncertainty of the age estimates. A 2016 study radiocarbon-dated the proteins in the eye-lens nuclei of 28 female Greenland sharks. Its largest animal, measuring 5.02 metres, had a midpoint age estimate of 392 years and a 95.4 percent probability range from 272 to 512 years.
As ScienceBlog has explained in detail, the animal was not known to be exactly 392. The 240-year range matters. Yet even its lower edge would place the shark’s birth decades before the First Fleet’s 1788 arrival.
The new vision study did not radiocarbon-date each animal’s lens. Ages were estimated from total body length using a growth model based on the earlier work. The oldest specimen in the new analysis was estimated to exceed 130 years.
That is old enough to test long-term retinal maintenance, but it is not the same as directly examining the retina of the famous 5.02-metre shark. The historical comparison describes the species’ demonstrated longevity range, not the known biography of the animals used in the new experiments.
A retina made for faint light
Most vertebrate retinas use two broad kinds of photoreceptor. Cones work best in brighter light and support colour discrimination. Rods are far more sensitive and dominate vision at night or in the deep sea.
The Greenland shark retina examined by the team was pure rod. Its rods were densely packed and elongated, features that increase the opportunity to catch scarce photons. The inner retinal layers were comparatively thin, resembling other deep-dwelling or nocturnal sharks.
The researchers could identify every major retinal layer: the photoreceptor layer, outer nuclear layer, inner nuclear layer and ganglion-cell layer. There was no obvious thinning or breakdown that would point to advanced retinal degeneration.
A DNA-fragmentation test provided another check. Untreated retinal sections showed no cells positive for TUNEL staining, which detects a hallmark of apoptosis and other cell death. A deliberately damaged positive control responded as expected.
That experiment was performed on sections from one animal, so it cannot establish that every old Greenland shark retina is free of ongoing cell death. It does show that well-preserved structure was not merely an empty arrangement of visibly degraded cells in that specimen.
The circuit was present and switched on
An intact-looking retina could still be biologically silent. To ask whether the circuitry remained active, the researchers used fluorescent RNA probes for the markers of its main cell types.
They detected rods, rod bipolar cells, GABAergic and glycinergic amacrine cells, Müller glia and retinal ganglion cells. Together, these populations form the route by which a light response is processed and sent toward the brain.
Chromatin markers also showed active and repressed regions in the nuclei across the retinal layers. That organisation is consistent with ongoing transcription and cellular metabolism, rather than a tissue preserved only in appearance.
Genome analysis found functional copies of the full complement of genes required for rod phototransduction. Retinal RNA sequencing from three Greenland sharks showed that key rod genes were being expressed at levels comparable with those in several other adult shark species.
Many genes associated with cone-based bright-light vision had become pseudogenes or were not expressed. This is not evidence of general blindness. It is the molecular signature of an eye specialised for scotopic, or low-light, vision.
A visual pigment tuned to Arctic blue
The researchers went beyond identifying the rhodopsin gene. They expressed the Greenland shark’s rod opsin in cultured cells, combined it with the light-sensitive molecule retinal and purified the resulting pigment.
Its maximum absorbance was 458 nanometres. That is shifted toward shorter, bluer wavelengths compared with most shallow-water sharks and even with many other deep-sea species.
Water removes red and longer-wavelength light quickly. In deep, clear, high-latitude water, the light that remains is strongly blue-dominated. A pigment peaking at 458 nanometres is therefore a sensible match to the Greenland shark’s world.
The membranes around its light-sensitive structures may also be adapted to the cold. Greenland shark retinas contained an unusually high proportion of DHA and very-long-chain polyunsaturated fatty acids compared with bovine retinas. These lipids help maintain membrane properties and support tightly packed rhodopsin in conditions that would otherwise make membranes rigid.
This biochemical fit is another reason the functional interpretation is stronger than an anatomical photograph alone. The tissue contains the cells, expressed genes, pigment and membrane environment expected for rod vision in deep Arctic water.
The parasite does not necessarily make the shark blind
Greenland shark eyes are often parasitised by Ommatokoita elongata, a copepod that anchors itself to the cornea. The conspicuous parasite helped produce a long-standing belief that these sharks must spend most of their lives blind.
The team measured light passing through six fixed corneas from five sharks. All had parasites attached around the corneal edges. Across wavelengths from 425 to 600 nanometres, the shark samples transmitted between 70 and 100 percent of the light.
In the blue range from 450 to 500 nanometres, transmission ranged from 66 to 100 percent. Fixed human donor corneas used for comparison averaged about 94 percent in that band.
These measurements do not recreate a complete living eye, nor do they show how an individual parasite affects the visual field. They do establish that parasitised Greenland shark corneas can remain highly transmissive. A parasite on the cornea is not automatically an opaque curtain.
The DNA-repair clue
Retinal neurons must maintain their DNA while remaining exposed to metabolic stress over an extraordinary span of time. The researchers therefore examined genes involved in repair, focusing on the ERCC1-XPF complex.
ERCC1 and XPF form an enzyme that cuts damaged DNA during several repair pathways. In humans and experimental animals, failures in this machinery are linked to sensitivity to ultraviolet light, accelerated ageing syndromes and retinal degeneration.
The longest-lived shark species in the comparison, including the Greenland shark, retained the ercc1 gene, whereas shorter-lived species in the selected group lacked it. Greenland shark retinas also expressed ercc4, the gene encoding XPF, at elevated levels compared with the other sharks.
This pattern suggests that robust repair may help retinal cells remain viable. It also echoes findings in another long-lived marine vertebrate. Recent bowhead whale research found unusually efficient and accurate repair rather than simply more tumour-suppressor barriers.
But similarity is not mechanism. The Greenland shark study did not disable ercc1 or ercc4, increase their activity experimentally, or follow retinal damage through time. Retention and elevated expression are clues. They do not yet show how much either gene contributes to visual longevity.
What cold water may contribute
Greenland sharks inhabit water as cold as minus 1.1 degrees Celsius and have exceptionally slow lives. Low temperature and low metabolic rate may reduce the pace at which some forms of molecular damage accumulate.
The study’s authors explicitly note this alternative contribution. A repair system does not work in isolation from the animal’s physiology, environment and evolutionary history.
The retina may be preserved by a combination of slower damage, effective repair, cold-adapted membranes and a visual system stripped back to the rod machinery its habitat rewards. The present data cannot assign a percentage to each part.
This also limits direct lessons for human ageing. A warm-blooded primate retina operating across bright daylight and darkness is not a Greenland shark retina living at depth. The genes are biologically relevant to both, but that does not make a shark adaptation a ready treatment.
A small study with unusually varied evidence
Rare, long-lived Arctic animals do not provide laboratory-sized samples. Retinal morphology was assessed in three adult Greenland sharks. Retinal transcriptomes came from three individuals, lipid measurements from two, and the detailed cell-marker and DNA-fragmentation assays shown in the paper used tissue from one.
The corneal analysis covered six corneas from five sharks. Comparisons with other shark transcriptomes were also complicated because species and life stage were not fully independent: some comparison animals were juveniles while others were adults.
Those limits make sweeping claims inappropriate. The strength comes from convergence. Tissue structure, named cell types, active rod genes, chromatin state, cold-suited lipids, a blue-sensitive pigment and transmissive corneas all point in the same direction.
The new study therefore does not prove that every Greenland shark sees sharply at 300 years old. It shows that the species has not simply abandoned vision in response to darkness, parasites or time.
An animal whose lifetime can overlap multiple centuries appears to keep the fundamental machinery of sight organised for at least its first 130 years. The repair genes may help explain how. For now, the intact retina is the finding; the molecular secret behind its endurance remains a question.