A Mad Scientist’s Dream – Rumpless Chickens (and more)

Today, we delve into the bizarre phenomenon of rumpless chickens—a feathered marvel characterized by caudal dysplasia, or as some like to call it, the ultimate chicken makeover! These quirky birds are missing their pygostyle, that charming little appendage known as the “parson’s nose,” a mutation that defies nature itself. This peculiar trait is inherited through an autosomal dominant gene—yes, you heard it right! One wild gene is all it takes to make a chicken strut around without its backside. The exact mutation responsible for this avian anomaly remains a mystery but fear not! Our intrepid scientists have proposed two tantalizing candidates for this genetic conundrum.

Imagine a laboratory filled with bubbling potions and beakers—where scientists don their lab coats and dive into the depths of genetic exploration. One such study by Nowlan H. Freese and colleagues in 2014 uncovered a novel gain-of-function mutation in the proneural IRX1 and IRX2 genes. These genes are crucial players in axis elongation during development, and their mischief leads to the delightful rumplessness we see in Araucana chickens, chickens with a genetic twist that would make even Frankenstein raise an eyebrow!

But wait! The plot thickens! In another feathered friend—the Piao chicken—a 798.5 kb deletion on chromosome 2 has been linked to this same rumpless trait. This deletion affects a newly discovered gene called Rum, which regulates MSGN1 expression, vital for mesoderm formation. It’s like a game of genetic Jenga—one wrong move and you’re left with a tail-less clucker!

Clucking around since time immemorial

These mad creations are not just confined to the laboratory; tailless fowl have been strutting their stuff (or lack thereof) for hundreds, possibly thousands of years. Our first documented sighting comes from the Italian naturalist Ulisse Aldrovandi. 

Picture this: It’s the year 1600, and while most of Europe is busy burning witches and inventing calculus, our dear friend Ulisse Aldrovandi is peering intently at chicken backsides. Yes, you heard that right! This Bolognese bird-brain (and I mean that as a compliment) penned the first known description of rumpless chickens in his magnum opus, “Ornithologiae Tomus Alter.” One can only imagine the excitement in his voice as he scribbled furiously, “Egads! These chickens have misplaced their buttocks!”

Pre-Columbian posterior peculiarities

But wait, there’s more! The Reverend J. Clayton spotted these tailless wonders in Virginia in 1693, though their origins remained a mystery. Some researchers believe these tailless wonders might have crossed the Pacific long before Columbus ever set sail. Imagine, if you will, intrepid chicken explorers, braving the vast ocean, their non-existent tails proudly… not wagging in the wind.

Fast forward to the early 20th century, and we find flocks of these tailless marvels in New York and Pennsylvania, serving as general-purpose fowls. But the rumpless revolution didn’t stop there! These birds were reported in Africa, Belgium (as the Walloon chicken), Ceylon, China, Japan, and even South America.

In 1925, the daring L.C. Dunn decided to dive deep into the derrière dilemma. In his groundbreaking work, “The inheritance of rumplessness in the domestic fowl,” Dunn unraveled the mystery faster than you can say “chicken butt.” He discovered that this tailless trait was passed down through generations like a family heirloom – if your family heirloom was a missing body part, that is!

Now, let’s talk Araucanas – the blue-egg-laying rumpless rockstars of the chicken world. The first Araucanas strutted into the United States in 1925, sporting their tufted, tailless look. But the real drama unfolded at the World Poultry Congress in 1921 in The Hague, where Dr. Salvador Castello introduced the Gallina Araucana as a new breed with three fabulous features: blue eggs, rumplessness, and ear tufts. But hold onto your feathers, folks! It turns out these Araucanas were actually a clever crossbreed created by Dr. Ruben Bustos, the patriarch of Chilean poultry keeping. He mixed two types of Chilean chickens: the ear-tufted with normal tails and the tailless without ear tufts.

So, there you have it, rumpless chickens – feathered oddities that remind us of the unpredictable magic of genetics, and a timeline of missing tails (and details), daring discoveries, and possibly the world’s first chicken sailors. Remember, in the world of mad poultry science, the absence of evidence is not the evidence of absence – especially when it comes to chicken rumps!

The question is whether caudal regression syndrome (CRS) or spina bifida in humans and rumplessness in chickens are related

Spoiler alert: the answer is a glorious “Sort of!” 

The Connection: A Tale of Caudal Woes

Both caudal regression syndrome in humans and rumplessness in chickens involve developmental anomalies affecting the caudal (tail-end) structures. In CRS, the lower spine and associated systems fail to develop properly, leading to absent or malformed sacral and coccygeal vertebrae. Similarly, rumplessness in chickens results in the absence of the pygostyle and caudal vertebrae. Superficially, these conditions seem like long-lost cousins at a family reunion of genetic oddities.

But the plot thickens: 

1. Causes in Humans (CRS):
   • CRS is linked to disruptions during embryonic development, particularly involving the notochord and mesoderm formation. It has been associated with maternal diabetes, teratogenic exposures, and mutations like those in the MNX1 gene (specific to Currarino syndrome).
   • Experiments have shown that teratogens like adriamycin or insulin can induce CRS-like anomalies in chick embryos.
2. Causes in Chickens (Rumplessness):
   • Rumplessness is inherited as an autosomal dominant trait and is caused by genetic mutations affecting developmental genes like IRX1, IRX2, or Rum. These genes disrupt axis elongation during embryogenesis.

Why They’re Not Quite the Same

While both conditions involve caudal malformations, CRS in humans is a broad syndrome with systemic effects (e.g., limb defects, genitourinary anomalies), whereas rumplessness in chickens is a localized phenotype affecting only tail structures. CRS arises from environmental or genetic disruptions during blastogenesis and neurulation, while rumplessness stems from specific genetic mutations tied to avian development.

Plot Twist

Here’s where it gets deliciously mad: researchers have actually induced rumplessness in chicken embryos using teratogens like insulin or adriamycin! This suggests that environmental disruptions can mimic genetic traits under experimental conditions. So yes, there’s a thematic connection between CRS and rumpless chickens—they both involve developmental derailments at the tail end—but the science says their underlying mechanisms are worlds apart…mostly.

We’ve all heard of insulin but what is this other teratogenic terror that bridges the gap between human syndromes and chicken curiosities, adriamycin?

Adriamycin, also known by its less sinister alias doxorubicin hydrochloride, is a powerful anthracycline antibiotic used in cancer chemotherapy. But in the hands of mad scientists (or in the wombs of unsuspecting test subjects), it becomes a molecular mischief-maker of the highest order! This DNA-disrupting dastardly drug works by inhibiting topoisomerase II, effectively throwing a wrench into the cellular replication machinery. It’s like telling your cells to build a skyscraper without a blueprint – chaos ensues! When administered to pregnant rats, Adriamycin produces a teratogenic smorgasbord of malformations, including:

1. Esophageal and intestinal atresia
2. Tracheo-esophageal fistula
3. Hypoplasia of the urinary bladder
4. Cardiovascular anomalies

But wait, there’s more! In the diabolical “Adriamycin rat model” (ARM), this chemical culprit can induce a whole host of VACTERL anomalies, including caudal regression! And in our feathered friends? Adriamycin can turn ordinary chick embryos into tailless wonders, mimicking the rumpless phenotype we so adore. It’s like a twisted game of genetic roulette, where the house always wins and the embryos always lose their tails!

The Spina Bifida Connection

While CRS and spina bifida are distinct conditions, they share some similarities in their impact on spinal development and associated complications:

1. Developmental timing:
   • CRS occurs earlier in embryonic development, typically before the fourth week of gestation.
   • Spina bifida develops when the neural tube fails to close properly around the fourth week after conception.
2. Affected areas:
   • CRS primarily impacts the lower (caudal) part of the spine, potentially affecting the sacrum, lumbar, and lower thoracic regions.
   • Spina bifida can occur anywhere along the spine but most commonly affects the lower back.
3. Associated conditions:
   • CRS is often associated with other syndromes like VACTERL and can affect multiple organ systems.
   • Spina bifida is primarily a neural tube defect but can be associated with other neurological and orthopedic issues.
4. Presentation:
   • CRS presents with a spectrum of spinal defects, from mild to severe, and may include sacral agenesis.
   • Spina bifida presents with various forms, including myelomeningocele (open spina bifida) and meningocele (closed spina bifida).
5. Overlap:
   • Some cases of CRS can present with spina bifida-like features, such as meningocele.
   • Both conditions can result in neurological deficits, bladder and bowel dysfunction, and lower limb abnormalities.
6. Risk factors:
   • Both conditions are associated with maternal diabetes and folic acid deficiency during pregnancy.

VACTERL is not merely an acronym – it’s a symphony of anatomical anomalies, a cacophony of corporeal conundrums! And it has shown up more than once in our notes so let’s dissect this, shall we?

V is for Vertebral vagaries, spinal shenanigans that would make a contortionist weep.
A stands for Anal atresia, a posterior peculiarity that gives new meaning to “backing up”.
C represents Cardiac capers, heart hiccups that keep cardiologists on their toes.
T and E, the dynamic duo of Tracheo-Esophageal tomfoolery, where eating and breathing play an anatomical game of twister.
R is for Renal riddles and Radial ruckus, because why have one body system affected when you can have two?
L stands for Limb librettos, appendages.

But wait, there’s more! Some throw an S into the mix for Single umbilical artery, because why not add another letter to this alphabet soup of anatomical antics? Sources say it is important to note that in about 75% of SUA cases, the baby is entirely healthy. However, the presence of SUA warrants additional prenatal monitoring and potentially more comprehensive neonatal evaluations and for a whole host of reasons. Increased risk of congenital anomalies: Babies with SUA have a 6.77 times higher risk for congenital anomalies. The most common associated anomalies are renal (6.48%), cardiovascular (6.25%), and musculoskeletal (5.44%). Chromosomal abnormalities: Neonates with SUA have a 15 times higher risk of chromosomal abnormalities. In high-risk populations, almost 20% of SUA cases are associated with chromosomal anomalies, with Trisomy 18 being the most common. Fetal growth and development: SUA is associated with an increased risk of fetal growth restriction, prematurity, intrauterine and intrapartum death. There’s also a higher incidence of small-for-gestational-age infants and pregnancy-induced hypertension. VACTERL association: SUA is found in up to 35% of patients with VACTERL association, often linked with kidney or urologic problems.

Now, here’s the kicker – to join this exclusive club of corporeal calamities, one must possess at least three of these malformations. It’s like a twisted game of anatomical bingo, where the prize is a lifetime of medical marvels!

Labyrinthine connections between brains and butts

In the feathered world of rumpless birds, the absence of those crucial caudal vertebrae and the uropygial gland isn’t just a cosmetic quirk – it’s a full-body experience that reaches all the way to their birdy brains! Without a proper tail, these avian oddities must rewire their neural circuitry to maintain balance and control flight. It’s like trying to fly a plane with the rudder missing – possible but requiring some serious cerebral gymnastics! The pièce de résistance of this posterior puzzle? The principles governing these tail-brain tête-à-têtes are eerily similar across the animal kingdom. From the lowliest worm to the haughtiest human, the neural nuts and bolts remain the same. It’s as if nature, in a fit of mad scientific fervor, decided to stick with a winning formula!

Now, let’s hop over to our human caudal conundrums. In cases of caudal regression syndrome, the brain doesn’t just shrug its neuronal shoulders at the missing bits. Oh no! Here too, the brain undergoes a fascinating rewiring act, adapting to the altered body map. This neural plasticity is like a cerebral game of Tetris, fitting the pieces together in a whole new way. In a marginally related twist that would make any mad scientist cackle with glee, human brain signals can command rat tails to twitch and twirl. It’s like a cross-species ventriloquist act, with our brains playing puppeteer to rodent rear ends!

The brain-to-tail connection isn’t just about motor control and body mapping. Recent studies suggest that the gut microbiome – yes, those tiny tummy tenants – might be playing a role in both avian and human caudal development. It’s like a microscopic puppet master pulling strings all the way from the gut to the brain to the tail (or lack thereof)!

The pygostyle, a peculiar posterior protuberance

In the grand scheme of avian evolution, the pygostyle is like nature’s way of saying, “Let’s streamline this tail situation.” But for our rumpless chickens, it’s more like nature threw out the blueprint and decided to freestyle.

The pygostyle isn’t just a bone to pick with chicken anatomy. Oh no, it’s a veritable Swiss Army knife of avian architecture! This “rump pillar” (as the ancient Greeks so poetically put it) is the backbone (pun intended) of the uropygium, that fleshy little football at the base of a bird’s tail. And what a multitasking marvel it is! Not only does it support tail feathers and muscles, but it’s also home to the uropygial gland, nature’s own bird beauty parlor.

Now, let’s talk about those rectrices, shall we? These tail feathers are the bird’s built-in rudder, helping our feathered friends brake and steer in flight. While most birds sport a respectable 12 rectrices, some grouse go absolutely bonkers with their tail feather count! It’s like they’re trying to compensate for something, eh? But what about our rumpless wonders? These posterior-challenged poultry are missing out on the whole tail feather party. It’s like showing up to a masquerade ball without a mask – scandalous! But who needs a tail when you can be the talk of the coop without one?

Now, let’s not forget the uropygial gland, that little oil factory nestled in the pygostyle’s loving embrace. This gland is the bird’s personal spa, producing a special oil that keeps feathers fabulous and flight ready. But our rumpless rebels? They’re going au naturel, baby! No preen gland, no problem – they’ve found other ways to stay fresh and fly, mostly by dust baths.

Falconer Emperor Frederick II wasn’t just whistling Dixie when he claimed the uropygial gland secreted a poison! While his theory of talon-delivered toxins was said to be off the mark, modern scientists have uncovered a far more diabolical truth!

These glands aren’t just oil factories. They’re microbial metropolises, teeming with bacteria that would make a microbiologist’s head spin! We’re talking about bacterial bad boys like Enterococcus and Corynebacterium setting up shop in these feathered fortresses. These bacterial boarders aren’t freeloaders – they’re paying rent in the form of antimicrobial warfare! That’s right, these microscopic mercenaries are pumping out bacteriocins and other antimicrobial compounds, creating a feathered force field against pathogens. Different bird species have their own unique bacterial battalions, tailored to their specific lifestyles and infection risks. Hole-nesters? They’re packing the heavy artillery. Open-nesters? They’re more of a lightweight division. But wait, there’s more! These glandular goodies don’t just stay put. Oh no, they’re spread far and wide during preening, turning the entire bird into a walking, squawking antimicrobial arsenal!

The uropygial gland: not just a simple oil dispenser, but a complex ecosystem of microbial mayhem, all working together to keep our feathered friends flying high and fungus-free! Who knew bird butts could be so fascinating?

Pygostyle As food

In the grand theater of American cuisine, the humble turkey tail has been unceremoniously booted off the stage. But fear not, for these fatty fannies have found fame and fortune in far-flung corners of the globe!

Picture this: It’s the 1950s, and U.S. poultry producers are scratching their heads, wondering what to do with mountains of turkey tails. Then, like a bolt of greasy lightning, inspiration strikes! “Let’s export these tailfeathers to the Pacific Islands!” And thus began the great turkey tail migration.

But why, you ask, did these tushy tidbits become treasures abroad? It’s simple – one nation’s trash is another’s culinary treasure! In places like Samoa, these fatty morsels became a cheap “protein” source (though they’re really more fat than anything else). Now, here’s where it gets juicy: Some countries, like Samoa, tried to ban these tailsome imports to curb obesity. But the World Trade Organization wagged its finger and said, “Nuh-uh! Free trade trumps health concerns!” But wait, there’s more! Turkey tails have found their way into pet food, with some claiming immune-boosting benefits for Fido. It’s like a cosmic joke – what’s bad for human health might be good for Rover!

The turkey tail: rejected by American plates, embraced by global palates, and possibly beneficial for our four-legged friends. It’s a story that truly embodies the phrase “waste not, want not,” or maybe just “Turkey ass. Eat up sucker.”

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This set of notes was inspired by an article which turned up in a search of older articles for ‘biotin’. The Insulin-induced abnormalities article showed up in an article about the effects of biotin deficiency. Both articles are from the 1940s.

Bonus goody that we didn’t fit into this tale of tails…The Greek word “οὐρά” (ourá) means tail. This ancient term is used to describe the rear appendage of animals like lions or dogs and even refers to the rear guard in military contexts. The word ourá and the word “aura” share a similar sound, but they don’t perfectly rhyme in all accents. In English, “aura” is pronounced more like /ˈɔːrə/ (AW-ruh), while “οὐρά” (ourá) is pronounced as /uˈra/ (oo-RAH) in Greek. However, if you pronounce “aura” with a slightly more emphasized “u” sound, as some people might, they could be said to rhyme.