Breaking free from the chains of the past Where
truth moves faster than a Holstein calf No law
waiting on some printed page We're charting new
ground in the digital age From genomic codes
to robot facts We cut through the noise, no hold
them back not your daddy's dairy news tonight
we're sparking Welcome back to the Bullvine Podcast,
where we cut through dairy industry noise to
get you the insights that actually matter for
your operation. And today, we're diving deep
into a feature piece that's got some serious
buzz. This one's got layers that'll make every
farmer really rethink their approach to color
genetics and the dominant red Holstein. It really
will, because, let's be honest, we all lived
by a very simple rule, the rule we learned in
high school biology. Red times red equals red.
It's, you know, it's Mendelian genetics 101.
It was simple. It was reliable. Exactly. And
that old comfortable rule, it's officially broken.
The discovery of the COPA gene back in 2015 introduced
a genetic override switch. That is, well, it's
fundamentally rewriting how color is transmitted
in Holsteins. And this isn't some abstract theory
in a lab. This is actively happening right now
in high -value breeding programs, and it's leading
to some major, major losses. The stakes here
are just astronomical, and this is why we're
hitting it so hard today. This isn't a discussion
about whether a show calf is, you know, pretty.
Not at all. We are talking about registration
errors that compound over generations. angry
buyers who feel completely misled, and ruined
reputations that take decades to build. Right.
If you're selling high -end embryos or donor
cows or heifers based on the promise of red genetics,
and those animals suddenly throw black calves
after you've mated them to other red animals...
You're losing serious money. We're talking tens
of thousands of dollars lost on a single flush.
And the core controversy here, this is the biggest
shocker, a variant red bull. A bull that looks
perfectly red can throw 50 % black calves. Even
when bred to a traditional recessive red cow.
A red sire, a red dam, and a black calf. We are
going to unpack the exact molecular mechanism
behind that financial trap today. And we're going
to explain why spending $30 on a specific genetic
test is currently the cheapest and frankly the
most necessary insurance policy you can buy in
your operation right now. So let's start by just
presenting the core issue. It's this red times
red equals black scenario. And it is absolutely
burning seed stock breeders who haven't caught
up with this research on the COPUS switch. We
see this playing out every day on the farm, especially
in operations that are really focused on marketing
the red and white color. So walk us through it.
A breeder sources what they think is a high quality
red bull. Right. They know he's a variant red,
which means he carries this copa gene. We call
him DRN, meaning he has one copy of the dominant
red variant and one normal one. Okay. And they
breed him to their proven recessive red cows,
which are the standard E at the traditional color
locus. So the expectation, based on what, three
generations of historical Holstein knowledge,
is 100 % red calves. Why wouldn't it be? Of course.
Both parents look red, they're fully registered
as red and white, and the dam has probably always
produced red calves. But the reality is... They're
getting exactly 50 % black calves instead. 50
%? It's a coin flip for color. And that's a coin
flip you just can't afford to lose if you are
marketing color. That's where the disaster starts.
And that's not an exaggeration. A disaster. No.
If I, the farmer... Sell a calf to a customer
who paid a premium, say, $5 ,000 for guaranteed
red genetics, and six months later it turns black,
or it's born black, or worse, I sell an embryo
guaranteeing red and the resulting calf is black.
My word is worthless. It's all about trust. In
the seed stock business, that trust and that
reputation damage, you can't quantify it, but
it's very real, and it takes years. if ever,
to recover. It doesn't matter how high the bull's
genomic numbers were if the fundamental promise
of the phenotype is broken. Okay, so let's strip
away the jargon and explain the mechanics simply,
because this is where the money is lost. The
COPA gene is the override. An animal can be genetically
programmed for black at the MC1R locus, that's
the traditional color switch on chromosome 18,
but if it carries the COPA variant, that dominant
red gene overrides the black signal and the animal
expresses red. So it looks red. We call it variant
red, or DR. So the bull looks red because the
copa switch is set to red override. But here's
the trap. The bull is hiding dominant black genetics,
the Eda Law allele, underneath. And he's almost
certainly E .D .E. that MC1R locus, just like
99 % of the black Holstein population. The copa
gene is just masking it. Precisely. The sire
is a black bull in red clothing, courtesy of
the copa gene. The surprise black calves happen
when the bull, who is heterozygous, DRN, at that
copa locus. He passes the N, normal allele. He
fails to pass on the override switch. Okay, let's
walk through the genetics of that specific calf.
The dam is recessive red, so she only has the
E allele to give at MC1R. Right, the calf gets
that E, no question. The sire is carrying the
dominant black allele, EDLRE, and if he's homozygous,
he's passing it. 100 % of the time. And crucially,
for the COPA gene, the calf gets the normal N
allele from that sire. That's the exact recipe
for disaster. That calf has no COPA override
because the sire didn't pass it on. And now,
the hidden dominant black gene, EELAO, is free
to express itself against the single recessive
red copy, the E the dam provided. And since E
dominates E? Boom! The calf is phenotypically
black, a black calf from two parents that look
completely red. And the breeder is left there
scratching their head thinking the recessive
red cow suddenly mutated or that the AI straw
was mislabeled. Yeah, they blame the AI company.
They blame the vet. They blame everything but
the real cause. And the problem was a lack of
knowledge about this COPA interaction. It's pure
chaos built on a simple misunderstanding of these
two color systems working in opposition. It's
brutal. If you sell 10 embryos at 500 bucks a
piece and half of them come back black, you're
refunding $2 ,500 instantly. And that's not even
mentioning the future business you just lost.
The math is just brutal when you miss that $30
test. To really appreciate how revolutionary
the scope of discovery is and why it changes
our breeding programs, we have to rewind a bit
and challenge the old paradigm. Right. For generations,
we focused exclusively on one thing, the MC1R
gene, the extension locus on chromosome 18. And
that gene determined whether the cow was making
black pigment, eumelanin, or red pigment, pheomelanin.
That was the key switch, period. That was the
baseline. And it was a beautifully simple model
for most of the breed's history. If you had dominant
black, EDO, you were black. End of story. And
if you wanted red, you needed two copies of recessive
red, the E genotype. Anything else was either
considered impossible or it was such a rarity
that breeders just ignored it. Let's quickly
review those MC1R alleles because... Differentiating
them is so crucial for understanding how this
COPA override works. Okay, so the standard is
EDIDL, dominant black. Over 99 % of Holsteins
carry this. It means the receptor is basically
locked on, constantly signaling for black pigment
production. Then you have recessive red, the
ELEL, and you need two copies. That'll dollars.
Right, and that's a severe frame shift mutation
that basically renders the MC1R receptor completely
non -functional. So since the receptor can't
receive that go black signal, the cell just defaults
to producing red pigment. It's a complete silence
of the black signal. It's off permanently. But
then we have to talk about the Telstar gene.
This caused massive confusion back in the day,
too. And it's so important we don't confuse it
with variant red. Oh, the classic disappearing
red. Exactly. Cavs carrying EBA. progeny of bulls
like roybrook telstar they're born red and you
cannot tell them apart from a true recessive
red calf at birth they look identical but between
three and six months of age their coats just
progressively darken you see mottled black hairs
start appearing and eventually the animal switches
fully to black and that switch it happens because
of an mc1r timing mechanism it's developmental
It is not related to the COPA transport system
at all. This is the critical differentiation.
Right. EBR is an MC1R allele that regulates when
the pigment switch happens. The ability to make
black pigment is there, but the switch is just
delayed. And we have to differentiate this visually
and genetically from the COPA effect. If you
skip testing, you could easily confuse a Telstar
-carrying calf with a variant red one at birth.
They look the same. But they have completely
different inheritance patterns and totally different
final phenotypes. Telstar animals always turn
black. Varroate red animals stay red, though
we'll get into how they might darken a bit later.
Okay, so that's the old, complicated system on
chromosome 18. Right. Now we introduce the copo
override, R160Cs, which sits on chromosome 3.
A completely different chromosome. Nowhere near
the traditional color locus, and yet it acts
as the master override switch. This is the definition
of epistasis. One gene controlling the expression
of another totally independent gene. So let's
use that Farmer English analogy again, but go
a little deeper into the biology, because this
mechanism is pretty fascinating. Let's do it.
Think of the melanocyte, the pigment cell, as...
A tiny specialized factory. For that factory
to start making black pigment, the eumelanin,
it needs two things. One, it needs the MC1R receptor
sitting on the outside of the cell ready to get
that go black signal. And two. Two, it needs
the specialized enzymes like tyrosinase or TYR
to be transported from the nucleus into the production
line, which is called the melanosome. So the
MC1R signal is the general manager shouting,
start making black paint. Because the animal
has the dominant black genetics, the EDLA. And
the COPA gene specifically, the protein complex
it codes for, which is COPI, is essentially the
internal delivery truck service inside that cell.
The delivery truck. I like that. The COPI complex
is responsible for transporting lots of proteins,
including these key enzymes and the MC1R receptor
itself, to the cell surface or the production
site. The specific mutation in variant red animals
is a defect that subtly disrupts this delivery
truck service. So it sounds like a really fundamental
problem. I mean, shouldn't that just kill the
cell if its delivery trucks are broken? That's
the incredible biological nuance here. The mutation
is severe enough to cripple the delivery of the
pigment -critical machinery. The paint and the
paint -making machines. Exactly. But it's mild
enough that it doesn't disrupt the general, you
know, housekeeping functions of the cell. The
cell survives just fine. So melanocytes, these
specialized pigment cells, they're just uniquely
sensitive to this slight disruption in the COPI
function. They need those delivery trucks to
be running perfectly to execute the black signal.
So the general manager, MC1R, might be screaming,
make black paint, because the animal carries
eight dollars. But the COPA gene has crippled
the delivery truck service. The required machinery
just doesn't reach the production line. The analogy
holds up perfectly. The COPA gene blocks the
delivery of the receptor to the cell membrane,
or it blocks the enzymes needed for the synthesis.
And without that working black machinery in place,
The cell defaults to its ground state, which
is producing pheomelanin, or red pigment. So
the animal is genetically signaling for black,
but the copa gene blocks the execution. That's
the genetic override, sitting on a completely
different chromosome. And this entire paradigm
-shifting discovery, which now costs or saves
breeders thousands of dollars, it all stemmed
from the impossible history of one cow. Surinam
sheik Rosabel Red, born way back in 1980. We
have to tell her story. We do. Rosabelle was
the paradox that the old science could not explain.
Her sire was confirmed ED -DA, homozygous dominant
black. So there was zero chance, under the traditional
MC1R model, that Rosabelle should have been anything
but black. Yet she was red. And she stayed red.
She was this anomaly that breeders and geneticists
argued about for years. Was it a spontaneous
mutation? Was the sire misidentified? The clincher
was when she was bred. She consistently produced
50 % red progeny, regardless of the black sire
that was used. That 50 % transmission pattern?
That just screams dominant trait entirely independent
of the MC1R locus. Exactly. If she were recessive
red, she could only pass on the E allele, and
when you breed that to a dominant black bull,
all her progeny should be black. But 50 % were
red. This proved the existence of an independent,
dominant red tree that was overriding the black
signal. Rosabelle was the foundation of variant
red, the real -world proof that this epistatic
interaction existed. Her genetics literally forced
geneticists to look beyond chromosome 18 and
find the COPA mutation on chromosome 3. It's
an incredible piece of detective work that directly
impacts the bottom line of every red and white
breeder today. Without Rezabel, we might still
be stuck in that red X red red mentality, just
losing money blindly. All right, let's bring
this discussion back down to earth and attach
some serious dollar signs to it. We're talking
genetics, transport proteins. The farmer driving
the tractor is asking, why should I spend $30
on yet another test? Because that $30 test is
your cheapest, fastest, most effective form of
insurance against thousands, potentially tens
of thousands in losses or major reputational
harm. The cost of the error here is just so disproportionately
high compared to the cost of getting the information.
The test, again, is a comprehensive color genotype.
It costs around 30 bucks through major labs like
UC Davis VGL. And crucially, it has to check
both COPA status. the variant red status, and
MC1R status, the extension locus. And if you're
using Holstein USA's standard genomic panels,
this data is integrated, but you have to know
how to read it. Okay, let's quantify the financial
risk. Let's look at four real -world scenarios
where skipping that $30 test results in a financial
catastrophe. Scenario 1, the Telstar trap. You
operate a seed stock business. You sell a beautiful,
high -genomic red heifer for $5 ,000, marketing
her as premium, true red breeding stock. You
skipped the $30 test because she looked red.
Of course. Six months later, she turns black
because she was carrying Iviar, the Telstar gen.
The customer contacts you, furious, demanding
a full refund. That is a $5 ,000 refund, plus
the loss of that customer for life and every
breeder they talk to. The heifer still has value
for milk, sure, but her value as a red breeding
animal, which is what the customer paid for,
it drops to near zero. Reputational damage among
show circles and red and white breeders is instantaneous.
You risk several thousand dollars to save 30,
it just doesn't pencil out. Never. Okay, scenario
two, the registration error. This one compounds
the damage across the entire breed. You have
a variant red calf, a DRN, looking identical
to a recessive red calf, EI2. You register it
as recessive red because, you know, the sire
was listed as red factor and the dam is red.
Right. Now that false pedigree data is locked
in the system, future buyers... maybe five years
down the line use that cow's genetics assuming
she's a clean recessive red line and their breeding
math is constantly wrong you're not just messing
up your own farm you're messing up everyone downstream
who relies on the accuracy of that pedigree and
if a buyer invests say $10 ,000 in a contract
for daughters from that line, and the resulting
calves fail to deliver the expected color. That
registration error is costing you potentially
massive liability and, again, huge reputational
recovery cost. Scenario three, the donor disaster.
This is where the losses get truly massive. Oh,
yeah. Imagine you have an elite black cow with
high genomics, a cow you want to convert into
red genetics. using a variant red bull, you decide
to flush her. You're spending, what, $4 ,000
to $6 ,000 on cinch, hormones, vet fees, recipient
cow management. All planning to sell the resulting
embryos for maybe $500 to $1 ,000 each, based
on a 50 % red guarantee. But if you made a false
assumption about the donor cow's hidden MC1R
status, or if your VRC bull wasn't fully tested,
those resulting embryos might not deliver that
promised red -black ratio. So you commit thousands
to the flush, and then you have to refund pre
-buyers. Or worse, the resulting calves are just
unsaleable because of a phenotype -genotype mismatch.
We're talking easily five figures lost, the cost
of the flush, the lost revenue on the embryos,
the time spent waiting, all because a $30 test
was skipped on the sire or the dam. And the final
one? Scenario four. The cleanup bull chaos. This
is the simplest financial trap. You turn out
a heterozygous variant, Red Bull DRN, and EBOL
for summer cleanup breeding in a mixed color
group. He's cheap, he's healthy, he gets the
job done. The calves are born, some red, some
black, some a little mottled. Now you've got
two problems. One, you have no idea which of
those red calves are recessive red and which
are variant red. And two, because you mixed colors,
you can't track the pedigree easily. So you need
to select replacements intelligently for the
next generation. But you can't tell the difference
just by looking at them. So what do you have
to do? Now you are forced into genomic testing
the entire calf crop, not just the keepers, just
to sort out the replacements and understand their
genetic value. At $30 to $40 per head for the
full color panel across dozens or hundreds of
animals. You've just spent thousands to clean
up the mess caused by skipping the initial $30
test on the bull. The chaos of phenotype ambiguity
forces you into expensive testing downstream.
So when you weigh a one -time $30 investment
against a $5 ,000 refund, $10 ,000 in lost embryo
sales, or $3 ,000 in unnecessary calf testing.
That $30 test is absolutely non -negotiable insurance.
If color is affecting your revenue stream, meaning
you are selling genetics, not just milk, you
cannot afford to guess. You need to know both.
the COPA status, and the underlying MC1R status.
Let's shift gears and talk about the strategic
appeal of Variant Red. I mean, why would any
breeder willingly introduce this level of complexity
and risk into their program? The answer is simple.
Speed and efficiency. That's the core appeal,
and it's why VRC is here to stay. Traditional
recessive red breeding is a generational commitment.
It's so slow. If you breed a heterozygous recessive
red cow, ED day, to a heterozygous bull, Edie,
you only get a 25 % chance of a red calf. It's
just hugely inefficient when you're trying to
inject color or any associated desirable redline
trait into an elite... black genomic line. Variant
red lets you do it fast. It's rapid integration.
Breeding a VRC bull to a high merit homozygous
black cow yields 50 % red calves in the first
generation. You instantly jumpstart the color
inheritance process. It makes the variant red
trait a really powerful strategic asset for commercializing
high genomic females from the black population.
And this trait was legitimized by specific animals
that combined that variant red gene with other
elite characteristics, particularly high type
and production. We have to talk about the matriarchs
that dragged VRC into the mainstream. We always
trace back to Rosabelle, the 1980 founder. But
the pivotal modern matriarch was Stoned and Fool's
Gold Red, born in 2007. She was sired by the
legendary Braydale Goldwyn and critically...
Fool's gold combined the dominant red gene with
show -winning type and high production index
numbers. She was a dominant female who brought
VRC into the mainstream genomic era. She made
it viable for breeders focused on profitability,
not just novelty. And that line continues right
through to modern sires. A great example is Vogue
Zircon P. He's a key modern carrier, heterozygous
DRN. But what makes Zircon P so strategically
valuable is what we call the double dominant
advantage. He also carries the polled trait.
That is a massive breeding tool. You are transmitting
two dominant market desirable traits, red and
polled, with a 50 % success rate for each in
a single generation straight into an elite black
line. That's how VRC moves from a genetic curiosity
to a strategic money -making asset. It's an instant
accelerator for specific traits. But now, the
nuance that gets breeders into trouble. The phenotypic
expression. We said VRC animals look red. But
we know they can darken. And this is where we
have to hammer home the difference between Telstar
and the VRC leaky blockade. Yes, we need to spend
time here. Because failing to distinguish these
two mechanisms is what leads to those registration
mistakes. Variant red expression isn't always
uniform and sable like the absolute non -functional
silence of a recessive red animal. The underlying
biology is completely different. Recessive red
is a broken receptor. It simply cannot make black
pigment. But variant red is a disrupted delivery
truck. that COPA defect that just slows down
the production of black pigment. And blockages,
especially biological ones, are inherently leaky.
Research confirms this. The inhibition of those
black pigment enzymes, TYR and TYRP1, in VRT
animals is less complete than it is in E -recessive
red animals. The cell is still trying to make
black pigment. And sometimes some of that machinery
gets through. especially as the animal matures
and hormonal balances shift. This explains the
famous Tecventuro calico red case. He was born
red, but he darkened significantly, eventually
turning mostly black later in life. And breeders
sometimes mistakenly assumed he was a Telstar
carrier because he darkened. But that darkening
is due to the inherent leakiness of that copa
blockade. over time, and it's potentially influenced
by testosterone, which is why darkening is often
more pronounced in bulls. The melanocytes manage
to synthesize enough eumelan to cause intermixed
black hairs or a darkening of the extremities.
They're just overcoming that transport blockage
slowly. It is absolutely crucial that breeders
understand this distinction. This VRC darkening
is not the Telstar mechanism, the EB gene. Right.
Telstar animals darken because their MC1R gene
is specifically programmed to switch on black
pigment production later in life. Calico Red
still transmits the dominant red gene, VRC. He
is darkening because his COPA mutation is an
imperfect block against the ED gene he carries.
Two different genetic processes. Similar visual
outcome of blackening, but completely different
inheritance patterns and breeding values. And
only testing tells the difference between the
red calf that will turn entirely black, that's
Telstar, and the red calf that will stay mostly
red but might darken at the extremities, which
is VRC. Okay, let's synthesize this into a practical
mating outcomes cheat sheet. If a farmer is using
VRC, what is the safest path and what is the
highest risk they absolutely have to avoid? The
cleanest, safest path to guaranteed red outcomes,
if you prioritize color consistency, is to use
a homozygous variant red sire, a DRDR bull. These
bulls are rare. We mentioned Vogue Red IP as
an example. But because they have two copies
of the override switch, they yield 100 % red
offspring, even on your homozygous black cows.
The override is guaranteed. Every single time.
This eliminates that 50 % risk. And the high
risk, high reward strategy. That's for the much
more common heterozygous variant, red sire, the
DRN, the zircon peas of the world. You have to
be surgical in their use. Use them aggressively
on your elite black dams, which are $80 at MC1R.
That's the strategic move. You instantly inject
red color into that pedigree with a 50 % hit
rate, and you accelerate your breeding plan.
And critically, do not, under any circumstances,
use them on your recessive red dams, your e -cock
cows. That is the precise mating we identified
at the very beginning that introduces the 50
% black calf risk, because you risked removing
the copa override by passing the N allele. and
exposing the bull's hidden dominant black gene,
AD dollars. If you are using a variant red bull,
you must know his underlying MC1R status. Is
he eated? If so, the risk is 50 % on your red
cows. It's all about risk management. If you
need guaranteed red, use DRDR or clean eGenetics.
If you're leveraging the speed of ERC, only mate
those DRN bulls to black cows. It's a simple
rule, but with massive implications. The industry
is clearly reacting to this newfound complexity.
The elite tier of genetics is already moving
toward mandatory COPA and MC1R testing at registration.
It's no longer optional. It's an inevitability
driven by the demand for transparency and accurate
pedigree data. Exactly. Competitive pressure
demands this clarity. When major AI studs, like
select sires, publish specific codes DR1, DR2,
and detailed mating guidance, they set the standard.
And breeders spending premium dollars on embryos
or semen demand to know exactly what they are
buying. If one supplier provides total genetic
transparency and the next one doesn't, the market
will always choose transparency. But here is
where the complexity gets international and where
breeders importing or exporting genetics can
get burned. Ah, yes. We need to decode those
standards because the names change depending
on which country you're dealing with. It's the
same genetics, just different shorthand. And
this can lead to massive expensive errors in
tag reanalysis. So in the U .S., the Holstein
Association and CDCB use DR0 for tested free,
DR1 for a heterozygous carrier, and DR2 for homozygous
dominant red. DR0, DR1, DR2. Got it. But if you
are looking at Canadian genetics... Holstein
Canada uses VRF for free, VRC for a carrier,
and VRS for a homozygous. VRF, VRC, VRF. Think
about a breeder in the U .S. purchasing semen
from a high genomic Canadian bull. The bull is
listed as VRC. If that U .S. buyer mistakenly
assumes VRC means variant red clean or somehow
confuses it with each genetics. They are introducing
a massive risk into their program. A VRC bull
in Canada is the same as a DR1 bull in the U
.S., a heterozytis carrier with that 50 percent
black risk when bred to a recessive red dam.
You absolutely must know which country's code
you are reading to prevent catastrophic breeding
mistakes. It requires a dedicated checklist at
the time of purchase. And this is just one example
of the increasing complexity that breeders have
to manage. It's not just about color, it's about
the fact that one mutation on chromosome 3 completely
overrides the effect of a gene on chromosome
18. This kind of network thinking is the future
of genomics across all traits. However, we have
to take a moment to acknowledge the holdouts
and their rationale is perfectly sound. We can't
just preach mandatory testing to everyone. Absolutely
not. For a large commercial 500 -cow dairy that
ships bull calves at a week old and selects replacements
purely on efficiency, milk production, and health
traits like feed saved. Color genetics are completely
irrelevant to their income statement. Right.
Mandatory testing across all registrations is
just... unnecessary friction, cost, and complexity
for those operations. Their rational business
decision is to prioritize traits that generate
revenue, which is milk, and reduce cost, which
is health and feed efficiency. They are maximizing
profit by ignoring color. We have to respect
that. The $30 test is irrelevant to them when
they are looking at $100 gain in health dollars
per animal per year. This deep dive is primarily
focused on operations that monetize genetics
and phenotype. Which brings us to the ultimate
verdict for anyone marketing genetics. Phenotype
alone is now useless in the Holstein breed. Wait,
that's a heavy statement. Unpack that again for
the farmer driving down the road. Phenotype alone
is useless for predicting genetic outcome. A
red calf at birth can be three fundamentally
different things, and you cannot tell the difference
just by looking at it. Okay, number one. One,
it could be variant red, VRC, or DR1. It carries
hidden dominant black. EDD2 and the dominant
override gene. Number two. Two, it could be recessive
red, EB2 exit. It is clean and transmits true
red. And number three. Three, it could be Telstar,
EE2. It will turn black in six months and may
carry the ED gene. They all look red at day one.
But only testing confirms which one. And that
distinction dictates the animal's future breeding
value, its marketability, and its potential to
wreck your mating program. If it's Telstar, it
turns black buyer beware. If it's BRC, it hides
black genetics breeder beware. If it's recessive
red, it's clean. That's the gold standard. It's
the ultimate lesson in modern genomics. You cannot
manage what you can't measure. The COPA discovery
didn't complicate color genetics. It just revealed
the complexity that had always been hidden beneath
the surface. It was always there. We just didn't
have the tools to see these epistatic interactions
before 2015. The breeders who adapt their programs
now, moving away from simple one -gene thinking
toward network analysis, are the ones who will
avoid those expensive surprises and, critically,
leverage the speed of the variant red trait strategically.
All right. A farmer just finished milking. pulled
out their phone and is driving to the feed store.
What are the three things they need to remember
and act on from today's discussion about the
COPPA switch? We need three actionable steps
based on clear timelines focused entirely on
protecting their investment. What's number one?
Immediate action this week. Immediate action.
Test your red sires. If you own, lease, or use
any variant red bulls or any red factor bulls
that trace back to the Roosevelt or Foles gold
lines, get their full color panel, COPA, and
MC1R now. This is your $30 insurance policy.
And the reasoning. You need to understand the
hidden dominant black genetics, the e -dealers
they are carrying. If that sire is DRN and e
-dealers, you know immediately that the 50 %
black calf risk exists when you mate him to any
recessive red cow you own. If you skip this,
you are betting thousands on a coin flip. What's
the medium -term strategy? Three to six months
out. Number two, rethink your red mating programs
and documentation. If guaranteed red calves are
your goal, especially for marketing high -value
heifers, stop relying on heterozygous variant
red, the DRN sires, on your red cows. The financial
risk of a failed calf or a refund is just too
high. So what's the alternative? Switch immediately
to using homozygous variant red, DRDR, sires
for guaranteed results, or... Use proven, tested
recessive red e -genetics that are confirmed
COPA -free, DR0 or VRF. And start documenting
the full COPA and MC1R status on all your replacement
heifers and animals you intend to market. Use
those breed standard codes clearly. Transparency
protects you from liability. And the long -term
positioning, one to two years down the road.
Number three, leverage VRC strategically, not
casually. Understand the actual strategic value
of variant red. Use the trait to convert your
highest genomic black females into red bloodlines
instantly. Mate your DRN bulls only to high merit
homozygous black cows to quickly produce valuable
50 % red daughters in the first generation. And
what should they avoid? Never, ever use VRC bulls
as cleanup bulls on mixed color groups during
the summer. The subsequent expense of sorting,
testing, and verifying those resulting calves
later, the thousands spent on genomic cleanup,
will wipe out any perceived breeding benefit.
Just stick to a clean, heat -recessive Red Bull
if you need a specific color cleanup. This has
been another deep dive from the Bullvine Podcast.
Managing complexity in dairy genetics is the
new reality, and the COPA switch is just the
first step in understanding how two different
genetic pathways affect our profitability. For
more straight -talking industry analysis, head
to www .thebullvine .com. Absolutely. The epistatic
interactions we saw today, one pathway overriding
another, they don't just stop at color. These
genetic networks show up in fertility, health,
and efficiency traits as well. The mental model
you build managing variant red is the same sophisticated
model you'll need for the next layers of genetic
complexity headed for your future breeding program.
It's all connected. It is. Subscribe wherever
you get podcasts. We're out with new episodes
every day, and next time's topic will be analyzing
how genetic networks like the epi - static interaction
we saw today show up in fertility, health, and
efficiency traits and what that means for your
future breeding program. We'll see you next time.