Key takeaways
- The published finding: E94K in MC1R was associated with dominant melanism in sampled wild Rattus rattus. [1]
- Breeder-recorded colony patterns: The breeder records E94K as incompletely dominant: heterozygotes (E/e) have a grey dorsum, with underlying agouti potentially visible on both belly and sides, and can rust towards agouti with age. Homozygotes (E/E) are jet black. The same agouti-showing and age-rusting pattern occurs in the darker parts of blonde rats that are also MC1R heterozygotes.
A black roof rat is striking, but the gene behind it is the genuinely interesting part. Coat colour in mammals is largely decided by a receptor called MC1R, one of the most studied genes in all of pigment biology, and the black roof rat sits at a rare and barely-studied end of it. Together with our agouti (wild type) and blonde rats, the black makes up a coat-defined allelic series in one tame, breedable colony, which is a real scientific resource. Here is the honest story of what the black coat is, what it might mean, and the popular claims about it that do not hold up.
A note on honesty: the established part is the gene. The interesting consequences are hypotheses, clearly flagged as such, and a couple of popular claims about black rats need a more careful hand than they usually get, which we try to give them.
What this changes about living with a black rat: nothing. The established thing on this page is a gene. Everything downstream of it, boldness, aggression, stress-resistance, is hypothesis, and nothing here is strong enough to be a reason to choose, pair, house, or handle any rat differently. That is not caution talking; it is what the evidence licenses. And there is a trap specific to this page: if you expect your black rat to be bold, you will see boldness, and by handling it as the bold one, you may even create it. So the honest move is the scientist’s move: change nothing, watch the animal in front of you without a verdict in mind, and let its coat predict nothing until the data can speak.
The switch, and its two ends
MC1R is the dial that decides whether a hair makes dark eumelanin (black and brown) or light pheomelanin (yellow and red). Turn the dial down and you get the light end: in people, the best-known low-function MC1R variants give red hair and fair skin. The black roof rat is the opposite end. In wild black Rattus rattus the black coat is an MC1R change called E94K, and the matching mouse receptor (E92K) is constitutively active, meaning it is stuck on without needing its normal signal.[1][2] So where the redhead is a turned-down receptor, the black rat is a natural always-on one. That is an unusual and useful thing to have in a live, breedable animal.
The mirror of the redhead
Almost everything we know about MC1R beyond colour comes from the turned-down (redhead) end, and it is not all good news. Low-function MC1R is linked to more vulnerable dopaminergic neurons, the cells lost in Parkinson’s disease, and to a real pain-signalling difference.[3] An always-on MC1R animal is the natural mirror of that, and the prediction runs the protective way: MC1R activation is anti-inflammatory (it is required for the calming effect of the hormone alpha-MSH in immune cells) and it switches on the Nrf2 antioxidant defences that protect neurons.[4][3] So a black roof rat may sit at the anti-inflammatory, antioxidant-protected end of an axis the field has mostly studied from the vulnerable end. This is a hypothesis, not a finding. The gain-of-function end has barely been studied in any mammal, which is exactly why a living one is worth having.
Two angles to handle with care
The honest-look matters as much as the hook. Two popular ideas about black rats need a careful hand for our gain-of-function rat.
Pain and painkillers. The famous MC1R pain finding is a loss-of-function effect (redheads need different doses of some painkillers). Our black is gain-of-function, the opposite direction, so we would not expect that same pain phenotype in it.[5]
Darker means bolder. Our black line did seem a touch more active, and that observation is real. What has changed is the picture behind it. MC1R is not pigment-only: the same receptor also sits on immune cells and in a few brain regions, so an always-on version has two honest receptor-level routes to behaviour without ever touching the adrenal gland. One is central, since an MC1R change already shifts central pain and opioid gating in the redhead.[5] The other is immune, since MC1R activation is anti-inflammatory and lowers the very cytokines that normally act as brakes on boldness.[3][4] That is more than we could say before. It still does not make the coat the cause. For a receptor-only allele the field’s own default is no temperament difference at all,[6] and the strongest competing explanation is not the receptor but its neighbours: in a small colony the black allele rides in a linked block of DNA, and the genes sitting next to Mc1r get selected along with the coat.[7] So we keep the observation as a genuine but still-unexplained pattern, and we hand the full case, and the test that could settle it, to our open research question on MC1R and temperament.
Could the effect run through the adrenal gland? A reader asked this directly, and it is a fair guess, because the adrenal is where the stress hormones are made. The clean answer is no, at least not from the coat. The adrenal cortex does not listen to MC1R at all. It runs on a different melanocortin receptor, MC2R, the one that answers ACTH, and MC2R will not even work until an accessory protein called MRAP escorts it to the cell surface.[8] The coat allele does not touch that system, so it cannot turn up adrenal steroid output. If anything the arrow runs the other way: chronically high ACTH can darken pigment a little through MC1R, which is why the skin darkens in Addison’s disease, but there the pigment is downstream of the adrenal, not upstream of it. So whatever the black coat does or does not do to temperament, it does not do it by way of the adrenal.
The plague question: plausible, unproven, and not what people think
The most famous thing about black rats is the plague, and a deeper idea sometimes rides along with it: that the plague itself selected for the black coat, which is why black rats supposedly became common in Europe. This one deserves a real answer rather than a dismissal, because part of it is plausible and part of it is simply untested.
Why it is plausible. MC1R is not only a pigment gene. The melanocortin system it belongs to is immune-active, and MC1R is specifically required for the anti-inflammatory action of the hormone alpha-MSH in immune cells.[4] A coat-colour gene that also tunes inflammation is exactly the kind of gene a deadly epidemic could, in principle, select on. The mechanism is real, and we are not going to tell you the idea is impossible.
And the two ideas need not compete; they may reinforce each other. Start with camouflage, but the concrete version, because the clue is in the name. The roof rat lives in the roof: the attic, the rafters, the underside of the thatch. In a medieval or early-modern town, homes were heated by open wood and coal fires with poor ventilation and few chimneys, and the smoke and soot rose and settled exactly there. Surviving medieval roofs have their timbers and the underside of the thatch encrusted with soot centimetres thick.[9] Against that blackened background a black rat is hidden and a pale agouti rat stands out to a cat or an owl. This is the peppered-moth story in a mammal, and centuries before the Industrial Revolution: when soot blackened the trees, the dark form of that moth was favoured because birds could no longer find it, the textbook case of selection by camouflage.[10]
And this is more than a just-so story. The dark morph is rare in the rat’s wild Indian homeland, where the animals are agouti;[11] in Turkey, the bridge between the two worlds, the black rats are the ones found in coastal towns and the upper floors of buildings while the agouti rats keep to fields and ground cover;[12] and feral ship rats that escape back into the wild, on remote islands, are agouti rather than black.[13] The dark coat tracks the dark indoor niche, not European geography as such, which is exactly what the soot-camouflage idea predicts.
Then the plague could reinforce it. Having seeded the dark coat through soot-matched crypsis in the rat’s own sooty niche, plague could then have acted on that already-dark city population: if the melanistic gene let infected rats tolerate the infection and live longer, those rats would be favoured by selection and, just as importantly, would make better reservoirs and vectors, carrying and spreading the bacterium for longer before they died, which would select the dark coat harder still. That is a self-reinforcing loop, not an either-or, and plague biology makes it concrete: plague is maintained in the wild today by partially resistant black-rat reservoirs (the Madagascar rats survive it through a different gene, CCR5).[14] The sharp form of the question is whether the melanistic allele would give tolerance, meaning alive and still infectious (a better vector), rather than full resistance, meaning cured (a dead end); and the anti-inflammatory MC1R tone, if it does anything here, would point toward tolerance.
Why it is still unproven. The integrated version is elegant, and it is also the most demanding, because it stacks several steps that each need checking: that European melanism is the same E94K allele (the one genetic study sampled Asian rats, found it rare and recent there, and made no European claim[1], and melanism is not even the same gene in a closely related species[15]); that the allele confers tolerance and not just colour; and that episodic plague selection was strong enough to matter against the repeated, trade-driven turnover of Europe’s rat populations (which arrived in distinct waves and were reshuffled by founder effects and drift).[16] The plague-resistance gene researchers have actually found in black rats is CCR5, a different one, which constrains but does not exclude a role for MC1R. And the starting premise, that black rats are specifically more common in Europe, is better described as an urban association and has never been quantified cleanly. There is also a deeper uncertainty in the plague leg itself: some archaeologists argue that rats were not even the main carrier of the medieval plague in northern Europe, where human fleas and lice may have done much of the spreading,[17] which would blunt any plague selection on rats there.
So the honest verdict is not proven, not disproven, and mechanistically plausible, and the both-at-once version is the most interesting thing to test rather than to assert or dismiss. The first concrete step toward testing any of it is to confirm the E94K allele in our own black rats, below.
A third possibility, and the one our own rats could settle
There is a third way the dark coat could have won, and it is the one we are best placed to test. The MC1R gene sits inside the melanocortin system, which across many animals is tied not only to colour but to boldness, stress resistance, and energy balance.[6] So a black rat might come with a quieter package: calmer and bolder around people, slower to stress, thriftier on the patchy food of a human larder. In a home or a granary, with predators gone, traits like those would favour the black coat on their own, with no need for soot or plague at all, and because the advantage would ride on behaviour rather than on pigment, it could push the coat to dominance without leaving much of a mark on the colour gene itself. Whether such an advantage is caused by the black gene or merely travels with it is an open question, and an important one.
That possibility is still open: a calmer or bolder or thriftier black rat is one honest way the dark coat could have spread. What we have to be disciplined about is the default. For a receptor-only change the field’s expectation is no behavioural difference, and if there is one, the first suspect is not the receptor but its neighbours. The black allele does not travel alone. It rides in a linked stretch of chromosome, and the gene right next door, TUBB3, is a neurodevelopmental gene that sits only a few kilobases from Mc1r and even shares transcription with it.[18] Select the coat in a small colony and you drag that whole neighbourhood along with it.[7]
This is also why the obvious test is not enough. Raising black and agouti littermates side by side does not separate the receptor from its neighbours, because siblings that differ at the coat differ across the entire linked block too. To actually pull the two apart we need blinded scoring and breeding across several generations to recombine that neighbourhood (or, one day, a clean knock-in of the single letter). That is our colony’s real job here, and it is the kind of work only a breeding colony can do. The full question, the competing explanations, and the test laid out in order live in our open research question on MC1R and temperament.
The allelic series, and the blonde connection
Here is where our colony becomes genuinely rare. It carries three named pigment genes in one tame, breedable line: agouti (wild type), blonde (a PCR-confirmed Rab38 null), and black (the MC1R gain-of-function allele), plus the melanistic-blonde double. That is a coat-defined allelic series, a living teaching and research resource that is hard to find anywhere else.
The two genes even interact. Our melanistic blonde rats run noticeably darker than non-melanistic blonde rats, which fits the idea that the always-on MC1R drives extra eumelanin and partly rescues the Rab38 pigment dilution.[19] Whether that also protects the light-sensitive blonde eye is a further open question. The blonde gene (Rab38) has two of its own deep dives, on ergothioneine and on ambroxol; the black gene is the third corner of the same triangle.
Open questions, and the tests that would settle them
Several clean questions come straight out of this. The first is the one we would run before any other, because it turns the whole story from likely into confirmed.
[G2] Is the colony’s black coat the constitutively active MC1R allele, and does PCR confirm E94K in our black rats?
Our rats are uniquely suited to answer this.
Where it stands: Black in wild R. rattus is the Mc1r E94K allele, and the homologous mouse E92K receptor is constitutively active. Our blonde is PCR-confirmed for Rab38, but our black is not yet sequenced for E94K, so confirming it is the first thing to nail down.
The test: Sequence Mc1r in the colony’s black rats and check for the E94K (G280A) substitution that Kambe found in wild black R. rattus.
What you would see if it holds: Our black rats carry E94K, confirming a natural gain-of-function (always-on) MC1R, the genetic mirror of the loss-of-function redhead that the pigment-genetics field studies almost entirely from the loss-of-function end.
What would falsify it: No E94K, which would mean a different gene drives black in this line. Melanism is not always MC1R; in the Okinawan Rattus tanezumi it is not.
Sources: Kambe Y et al. 2011, Zoological Science 28:560-567[1]; Benned-Jensen T, Mokrosinski J, Rosenkilde MM 2011, PLoS ONE 6:e24644[2]; Kambe Y et al. 2012, Genes & Genetic Systems 87:29-38[15]; Sasamori S, Yoshida MA, Suzuki H, et al. 2017, Zoological Science 34:513-522[20].
[G3] Does the always-on MC1R in black roof rats put them at the anti-inflammatory, Nrf2-protected end of the pigment-immunity axis?
Where it stands: MC1R activation is anti-inflammatory and drives Nrf2 neuroprotection, and loss-of-function redheads are more vulnerable (they lose more dopaminergic neurons). A constitutively active MC1R mammal would be a natural always-on version, which has not been studied. Two related angles need a careful hand rather than a dismissal: the redhead pain and analgesia phenotype is a loss-of-function effect, so it points the opposite way from our gain-of-function black and we would not expect it here; and the darker-equals-bolder behaviour idea is plausible but hard to pin on MC1R itself, because the colour-and-behaviour link in animals usually runs through shared melanocortin ligands rather than the receptor, so the observation stands as real but unexplained.
The test: Challenge black (gain-of-function MC1R) and agouti roof rats with a standard inflammatory or oxidative stressor and compare inflammatory markers, Nrf2-pathway activity, and neuron survival.
What you would see if it holds: Black rats show a blunted inflammatory response and stronger Nrf2 antioxidant defense, the gain-of-function mirror of the redhead, who sits at the vulnerable loss-of-function end.
What would falsify it: No difference, or black rats fare worse, which would mean the coat allele does not carry the predicted protective tone in a live animal.
Sources: Chen X, Chen H, Cai W, et al. 2017, Annals of Neurology 81:395-406[3]; Mogil JS, Wilson SG, Chesler EJ, et al. 2003, Proceedings of the National Academy of Sciences 100:4867-4872[5]; Ducrest AL, Keller L, Roulin A 2008, Trends in Ecology & Evolution 23:502-510[6].
[BH11] Do black roof rats, assuming their black coat is the constitutively active MC1R E94K allele (question [G2]), differ in temperament from their agouti siblings, bolder and quicker to escalate when provoked? And if they do, is it the coat receptor itself acting outside the skin, or a neighbouring gene dragged along with it on the chromosome?
Our rats are uniquely suited to answer this.
Where it stands: Across many vertebrates darker, more eumelanic animals tend to be bolder, more aggressive and more stress-resistant, and the usual explanation is that pigment and temperament are co-regulated by the shared melanocortin (POMC) system, in which the same peptides (alpha-MSH, ACTH, and the antagonist ASIP) that set coat colour also tune behaviour and the stress axis across the five melanocortin receptors. But that covariation is ligand-driven, and our case is different and harder, because our black is a coding change in ONE receptor, MC1R, and the researchers who built the pleiotropy idea (Ducrest, Keller and Roulin) treat MC1R as the exception to it, largely melanocyte-restricted. So for a receptor-only change the disciplined prior is NO temperament difference, and a real difference would be the surprising, high-bar finding rather than the expected one; the wild darker-equals-bolder pattern is itself only influential, not settled, since a 2024 meta-analysis found colour-behaviour associations are real overall but not specific to melanin. On the adrenal question the answer is clean: the coat allele cannot reach the adrenal directly, because the adrenal cortex runs on a DIFFERENT melanocortin receptor, MC2R, which responds only to ACTH and needs the accessory protein MRAP even to reach the cell surface, while MC1R does not drive steroid output (if anything the arrow runs the other way, since chronically high ACTH can weakly darken pigment through MC1R as in Addison’s disease, but pigment does not drive the adrenal). What keeps a receptor-level effect on the table is that MC1R is not pigment-only: it also sits on immune cells (macrophages, microglia) and in specific brain regions such as the periaqueductal gray, giving a constitutively active E94K two receptor-intrinsic routes. First, a central one, since an MC1R change already alters central sensory and opioid gating (the loss-of-function redhead has altered pain and analgesia), so an always-on receptor could shift reactivity; second, an immune one, since MC1R activation is anti-inflammatory (it suppresses NF-kB and lowers cytokines such as IL-1beta and IL-6) and those same cytokines are the brakes that normally induce caution and behavioural inhibition, so a permanently anti-inflammatory MC1R could lift them (our question [G3] carries this immune angle, and is also why the effect cannot simply be pinned on the receptor). The E94K allele is a constitutively activating gain-of-function, the same class as the mouse sombre and tobacco E92K, which signals (biased cAMP and arrestin recruitment) without its ligand, so if any of these routes matter this is the genotype that would show it. The shape Brian sees fits a known ethology: in coping-style terms boldness and provoked aggression are two faces of one ‘proactive’ type, and the step from bold to aggressive is conditional rather than fixed, since in sticklebacks the boldness-aggression correlation appeared only after the fish had met a predator, so a black rat that reads as merely bold at rest and escalates mainly when provoked or already in a bad mood is exactly that predicted shape. The honest brake is the strongest competing explanation, and it is not the receptor: in a small closed colony the black allele rides in a haplotype, and genes physically next to Mc1r are dragged to high frequency with the coat when it is selected (genetic hitchhiking), while the Mc1r neighbourhood is dense with neuro and immune genes (the neurodevelopmental gene TUBB3, Class III beta-tubulin, sits only a few kilobases downstream of Mc1r and is even co-transcribed with it). A littermate design does NOT break this, because siblings that differ at the coat also differ across the whole linked block, and the murine tell points the same way, since the dark sombre and tobacco E92K mouse is not reported as notably aggressive, which argues against the receptor causing the temperament by itself. So a linked neighbour, not the receptor, is the disciplined default until breeding or a knock-in can separate them. What is genuinely open is whether black and agouti animals actually differ here, which is untested, and this colony is unusually placed to test it, with a single, PCR-confirmable allele (MC1R E94K, pending confirmation in [G2]) segregating in tame, handleable siblings; Brian tracks it in the colony’s black-versus-agouti study, and a second breeder in the collaboration independently reports the same direction, a blonde rat carrying the black MC1R allele being more aggressive than a blonde without it.
The test: Score tameness, boldness and exploration (open field, elevated-plus-maze), and provoked aggression (a resident-intruder or tube-dominance test) in black versus agouti animals, with the scorer BLINDED to coat colour (coat-masked video, or a rater who cannot see the animal), because an unblinded ‘the blacks are meaner’ impression is expectancy-laden and would not survive review. Treat litter and dam as the statistical unit (a mixed model with litter as a random effect), since pups in one litter are not independent. Then separate the receptor from its neighbours: do not rely on littermates alone, because siblings that differ at the coat also differ across the whole linked chromosome block, but breed black by agouti across several generations so recombination can uncouple the coat from adjacent genes, then test whether temperament tracks the MC1R allele or the coat block. The decisive versions are a cross-population test (does an independently arisen E94K line show the same temperament?) or a CRISPR knock-in of E94K on a clean, uniform background. Reading the stress axis (baseline and post-handling corticosterone) can place any difference on the proactive-reactive map, but a stress-axis difference is downstream, not proof of the mechanism.
What you would see if it holds: Black animals are reliably bolder and quicker to escalate under blinded scoring, AND the temperament still tracks the MC1R allele after recombination has broken the linkage (or in a knock-in). That would be a rare demonstration of receptor-level melanocortin pleiotropy from a single, known gain-of-function allele, the always-on mirror of the loss-of-function redhead, and would most plausibly run through MC1R’s jobs in the brain and immune cells rather than the adrenal.
What would falsify it: Two ways. If blinded scores show no black-versus-agouti difference, the coat allele carries no temperament corollary here, consistent with the receptor-restricted view in question [G3]. If a difference exists but does NOT track the MC1R allele once recombination breaks the linkage block (or fails to reappear in a knock-in), then a hitchhiking neighbour, not the receptor, was driving it.
Sources: Ducrest AL, Keller L, Roulin A 2008, Trends in Ecology & Evolution 23:502-510[6]; Roulin A, Ducrest AL 2011, European Journal of Pharmacology 660:226-233[21]; Ruckman SN, Humphrey EA, Muzzey L, Prantalou I, Pleasants M, Hughes KA 2024, Ecology and Evolution 14:e70655[22]; Mafli A, Wakamatsu K, Roulin A 2011, Animal Behaviour 81:859-863[23]; Almasi B, Jenni L, Jenni-Eiermann S, Roulin A 2010, Journal of Evolutionary Biology 23:987-996[24]; Kambe Y et al. 2011, Zoological Science 28:560-567[1]; Benned-Jensen T, Mokrosinski J, Rosenkilde MM 2011, PLoS ONE 6:e24644[2]; Mogil JS, Wilson SG, Chesler EJ, et al. 2003, Proceedings of the National Academy of Sciences 100:4867-4872[5]; Chen X, Chen H, Cai W, et al. 2017, Annals of Neurology 81:395-406[3]; Koolhaas JM, Korte SM, De Boer SF, Van Der Vegt BJ, Van Reenen CG, Hopster H, De Jong IC, Ruis MA, Blokhuis HJ 1999, Neuroscience & Biobehavioral Reviews 23:925-935[25]; Bell AM, Sih A 2007, Ecology Letters 10:828-834[26]; Maynard Smith J, Haigh J 1974, Genetical Research 23:23-35[7]; Dalziel M, Kolesnichenko M, das Neves RP, Iborra F, Goding C, Furger A 2011, Nucleic Acids Research 39:2378-2392[18].
[G6] Why did the melanistic (MC1R E94K) coat become common in commensal black rats: relaxed predation plus founder drift indoors, soot camouflage, plague tolerance, or a commensal-fitness syndrome (bolder, lower-stress around people, thriftier metabolism) carried with the black allele?
Our rats are uniquely suited to answer this.
Where it stands: The genetics are largely settled (pending peer review for the European samples): black is the dominant MC1R E94K gain-of-function allele, of a single recent origin, that hitchhiked on the commensal lineage out of Asia, and it is an indoor-commensal trait, not a European one (agouti dominates the wild native range and feral island populations, while the black morph tracks buildings and attics). The open part is the SELECTION. In the wild, dark coats are purged by predators, which is why natural populations stay agouti; indoors that penalty is relaxed, soot-blackened attics may even make a dark rat cryptic (the pre-industrial peppered-moth idea), and founder effects and drift in isolated city and ship populations push the allele up. A preliminary genomic analysis reportedly finds no strong selection signature on the coat-colour gene itself, consistent with relaxed selection plus drift rather than a hard sweep. On top of that, the melanocortin system MC1R belongs to is pleiotropic, linked across species to boldness, stress resistance, and energy balance, so if the black allele also carries (or co-segregates with) a commensal-fitness advantage, calmer and bolder around people and thriftier on patchy human food, that would favour black in the human niche even with predators gone, and a behaviour-linked advantage need not leave a signature on the pigment gene. Whether such an advantage is caused by the MC1R change or merely linked to it is open. The plague could add an episodic reinforcing push where rats were the vector (itself debated for medieval northern Europe). Brian notes black is the dominant coat in our own colony.
The test: In our colony, where black is dominant and we already select for calmness around people, raise black and agouti littermates together in a common predator-free indoor environment and compare boldness and handling tolerance, stress physiology (cortisol, adrenal size), and weight gain and feed efficiency on a standard ration; PCR-confirm the E94K allele and test whether it tracks any behavioural or metabolic difference. Historically, map melanistic frequency against plague geography and indoor-soot exposure, and replicate the genomic selection test in peer review.
What you would see if it holds: Black littermates are consistently bolder, lower-stress, or thriftier than agouti littermates in a predator-free indoor setting, showing a commensal-fitness advantage of the allele (or of variation linked to it) that selects for the dark coat independent of camouflage and plague.
What would falsify it: Black and agouti littermates are indistinguishable in temperament, stress, and growth, leaving relaxed predation, soot camouflage, founder drift, and the debated plague leg as the only candidates; or the genomic neutrality result holds with no niche advantage found, making drift the main story.
Sources: Li D, Taylor AW 2008, Journal of Leukocyte Biology 84:191-198[4]; Kambe Y et al. 2011, Zoological Science 28:560-567[1]; Kambe Y et al. 2012, Genes & Genetic Systems 87:29-38[15]; Tollenaere C, Rahalison L, Ranjalahy M, et al. 2008, Infection, Genetics and Evolution 8:891-897[14]; Letts JB 1999, English Heritage / University of Reading[9]; Cook LM, Grant BS, Saccheri IJ, Mallet J 2012, Biology Letters 8:609-612[10]; Pagès M, Corbet G, Orth A, Volobouev V, et al. 2011, Journal of Mammalogy 92:659-670[11]; Yiğit N, Çolak E, Kandemir İ, Kankılıç T 2008, Zoology in the Middle East 45:19-28[12]; Gales RP 1982, New Zealand Journal of Zoology 9:463-466[13]; Hufthammer AK, Walløe L 2013, Journal of Archaeological Science 40:1752-1759[17]; Ducrest AL, Keller L, Roulin A 2008, Trends in Ecology & Evolution 23:502-510[6].
Common questions
Is a black roof rat the same as a black fancy rat?
The colour looks similar, but the genetics are not the same. Black in the wild roof rat (Rattus rattus) comes from a gain-of-function change in the MC1R gene, an always-on pigment switch. Black in fancy rats (Rattus norvegicus) is usually the non-agouti gene, a different mechanism. So a black roof rat is its own thing, not a roof-rat version of a black fancy rat.
Did black rats really cause the Black Death because of their colour?
Black rats mattered to the plague as hosts for the infected fleas, and that part is real. The deeper idea, that plague itself selected for the black coat, is a genuine open hypothesis, not a settled fact in either direction. It is mechanistically plausible, because the MC1R gene behind the black coat is also immune-active, and it need not compete with the camouflage explanation: a dark city rat that tolerated plague would both survive longer and spread it more, so the two pressures could reinforce each other. But there is no direct evidence it happened, the melanism allele has only been studied in Asian rats, and the plague-resistance gene actually found in black rats so far is a different one (CCR5). So: plausible, unproven, and worth real study, not something to assert or to dismiss.
Are black roof rats more aggressive or more active?
People sometimes say so, and our own line did seem a bit more active. That observation is real, but it is confounded (different source populations, different breeding history) and hard to pin on the MC1R coat switch itself, because the colour-behaviour link in animals usually runs through shared signalling molecules rather than the receptor. So we keep the observation as a genuine but unexplained pattern, and we just do not claim the gene is what causes it.
Is the black colour healthy?
Yes. Unlike the blonde coat, which knocks out a gene with real downstream effects, the black coat is a gain-of-function pigment change, and if anything the interesting hypotheses point the protective way (anti-inflammatory, antioxidant). Those are unproven predictions, not promises, but there is no health downside to a black coat that we know of.
Go deeper
Related: Coat colour and genetics (the overview) · Ergothioneine and the blonde rat · Ambroxol and the blonde rat · All open research questions.
This page describes established genetics and the open hypotheses around it, clearly labelled. Open hypotheses are ideas with a test attached, not facts. We have nothing to sell; the colony exists to keep these rats and this knowledge going.
References
- [1] Kambe Y et al. “Origin of agouti-melanistic polymorphism in wild black rats (Rattus rattus) inferred from Mc1r gene sequences.” Zoological Science 2011;28:560-567. PubMed.
- [2] Benned-Jensen T, Mokrosinski J, Rosenkilde MM. “The E92K melanocortin 1 receptor mutant induces cAMP production and arrestin recruitment but not ERK activity indicating biased constitutive signaling.” PLoS ONE 2011;6(9):e24644. PubMed.
- [3] Chen X, Chen H, Cai W, et al. “The melanoma-linked “redhead” MC1R influences dopaminergic neuron survival.” Annals of Neurology 2017;81(3):395-406. PubMed.
- [4] Li D, Taylor AW. “Diminishment of alpha-MSH anti-inflammatory activity in MC1r siRNA-transfected RAW264.7 macrophages.” Journal of Leukocyte Biology 2008;84(1):191-198. PubMed.
- [5] Mogil JS, Wilson SG, Chesler EJ, et al. “The melanocortin-1 receptor gene mediates female-specific mechanisms of analgesia in mice and humans.” Proceedings of the National Academy of Sciences 2003;100(8):4867-4872. PubMed.
- [6] Ducrest AL, Keller L, Roulin A. “Pleiotropy in the melanocortin system, coloration and behavioural syndromes.” Trends in Ecology & Evolution 2008;23(9):502-510. PubMed.
- [7] Maynard Smith J, Haigh J. “The hitch-hiking effect of a favourable gene.” Genetical Research 1974;23(1):23-35. PubMed.
- [8] Metherell LA, Chapple JP, Cooray S, David A, Becker C, Ruschendorf F, Naville D, Begeot M, Khoo B, Nurnberg P, Huebner A, Cheetham ME, Clark AJ. “Mutations in MRAP, encoding a new interacting partner of the ACTH receptor, cause familial glucocorticoid deficiency type 2.” Nature Genetics 2005;37(2):166-170. PubMed.
- [9] Letts JB. “Smoke-Blackened Thatch: A unique source of late medieval plant remains from Southern England.” English Heritage / University of Reading 1999. link.
- [10] Cook LM, Grant BS, Saccheri IJ, Mallet J. “Selective bird predation on the peppered moth: the last experiment of Michael Majerus.” Biology Letters 2012;8(4):609-612. PubMed.
- [11] Pagès M, Corbet G, Orth A, Volobouev V, et al. “Morphological, chromosomal, and genic differences between sympatric Rattus rattus and Rattus satarae in South India.” Journal of Mammalogy 2011;92(3):659-670. DOI.
- [12] Yiğit N, Çolak E, Kandemir İ, Kankılıç T. “Allozyme variation in Rattus rattus (Rodentia: Muridae) in Turkey, with particular emphasis on the taxonomy.” Zoology in the Middle East 2008;45(1):19-28. DOI.
- [13] Gales RP. “Age- and sex-related differences in diet selection by Rattus rattus on Stewart Island, New Zealand.” New Zealand Journal of Zoology 1982;9(4):463-466. DOI.
- [14] Tollenaere C, Rahalison L, Ranjalahy M, et al. “CCR5 polymorphism and plague resistance in natural populations of the black rat in Madagascar.” Infection, Genetics and Evolution 2008;8(6):891-897. PubMed.
- [15] Kambe Y et al. “Genetic characterization of Okinawan black rats showing coat color polymorphisms of white spotting and melanism.” Genes & Genetic Systems 2012;87(1):29-38. PubMed.
- [16] Yu H, Jamieson A, Hulme-Beaman A, et al. “Palaeogenomic analysis of black rat (Rattus rattus) reveals multiple European introductions associated with human economic history.” Nature Communications 2022;13:2399. DOI.
- [17] Hufthammer AK, Walløe L. “Rats cannot have been intermediate hosts for Yersinia pestis during medieval plague epidemics in Northern Europe.” Journal of Archaeological Science 2013;40(4):1752-1759. DOI.
- [18] Dalziel M, Kolesnichenko M, das Neves RP, Iborra F, Goding C, Furger A. “Alpha-MSH regulates intergenic splicing of MC1R and TUBB3 in human melanocytes.” Nucleic Acids Research 2011;39(6):2378-2392. PubMed.
- [19] Oiso N et al. “The rat Ruby (R) locus is Rab38: identical mutations in Fawn-hooded and Tester-Moriyama rats derived from an ancestral Long Evans rat sub-strain.” Mammalian Genome 2004;15(4):307-314. PubMed.
- [20] Sasamori S, Yoshida MA, Suzuki H, et al. “Potential causative mutation for melanism in rats identified in the agouti signaling protein gene (Asip) of the Rattus rattus species complex on Okinawa Island, Japan.” Zoological Science 2017;34(6):513-522. PubMed.
- [21] Roulin A, Ducrest AL. “Association between melanism, physiology and behaviour: a role for the melanocortin system.” European Journal of Pharmacology 2011;660(1):226-233. PubMed.
- [22] Ruckman SN, Humphrey EA, Muzzey L, Prantalou I, Pleasants M, Hughes KA. “Assessing the Association Between Animal Color and Behavior: A Meta-Analysis of Experimental Studies.” Ecology and Evolution 2024;14(12):e70655. PubMed.
- [23] Mafli A, Wakamatsu K, Roulin A. “Melanin-based coloration predicts aggressiveness and boldness in captive eastern Hermann’s tortoises.” Animal Behaviour 2011;81(4):859-863. DOI.
- [24] Almasi B, Jenni L, Jenni-Eiermann S, Roulin A. “Regulation of stress response is heritable and functionally linked to melanin-based coloration.” Journal of Evolutionary Biology 2010;23(5):987-996. PubMed.
- [25] Koolhaas JM, Korte SM, De Boer SF, Van Der Vegt BJ, Van Reenen CG, Hopster H, De Jong IC, Ruis MA, Blokhuis HJ. “Coping styles in animals: current status in behavior and stress-physiology.” Neuroscience & Biobehavioral Reviews 1999;23(7):925-935. PubMed.
- [26] Bell AM, Sih A. “Exposure to predation generates personality in threespined sticklebacks (Gasterosteus aculeatus).” Ecology Letters 2007;10(9):828-834. PubMed.