There’s an incredible link between zebra stripes and how our fingerprints grow: ScienceAlert

No one on Earth has fingerprints like yours. Even if you have an identical twin, the spiral arrangement of ridges on your hands and feet will be unique to you.

Scientists had their suspicions about what factors might decide their unique pattern of impressions, but struggled to pin down the exact mechanisms.

Using a variety of procedures on mice, human tissues, cell cultures and genes, an international team of researchers has perfected the process that literally gives rise to our skin’s signature dimples.

The tiny bumps and furrows of skin found on human fingertips begin to form around the 13th week of a fetus’ life. The pattern that finally emerges from these colliding lines stays with a person for the rest of their days, persisting through virtually any kind of wear and tear.

Monozygotic twins are formed from the same egg and sperm, and yet when they are born, each twin has experienced its own set of genetic mutations in utero, which makes them 100% identical.

The odds of your fingerprints matching at birth is about 1 in 64 billion – an extremely low chance that has never been seen before.

Part of the reason twins have different fingerprints might have something to do with their slightly different genomes. But there are also many other subtle factors at play, such as the molecular pathways that share information and instructions between genes.

These are known as signaling pathways and are highly sensitive to tiny local factors within the womb, which means they work differently for everyone, even twins.

The current study, led by researchers at the University of Edinburgh, identified three different signaling chains in particular that appear to shape gripping in our fingers: Wnt, bone morphogenetic protein (BMP) and ectodysplasin A receptor (EDAR) pathways. All three were identified by observing the development of human cells in the laboratory. Its role was further tested in mouse models.

Rats don’t have fingerprints like we do, but they do have transverse ridges of skin on their fingers that develop in a similar way, albeit with less complexity.

In both humans and mice, Wnt pathways appear to stimulate the growth of furrows in the outer layer of skin on a finger, whereas BMP suppresses the formation of these furrows. EDAR signals, in turn, help shape the size and spacing of the cutaneous ridges that form.

When EDAR activity was silenced in mouse models, for example, their digits showed no transverse ridges, but a polka dot-like pattern.

The push-and-pull in ridge formation reflects patterns that emerge from what’s known as the Turing reaction diffusion system, and seems to be a big reason why our fingerprints end up looking so different.

A Turing pattern is a mathematical concept developed by Alan Turing in 1952 to explain how stripes and spots in nature show random, minute differences in their structure.

When two ‘diffusible’ substances collide, the Turing model shows that the result is not always the same. There’s a lot of noise and variability in how the collision ultimately plays out, resulting in chaos that’s hard to predict.

Like a zebra’s stripes, scientists believe this complexity is part of what leads to the “fine, richly detailed structure” in each of our fingerprints.

In humans, these bumps tend to form at the tip, bottom, and center of the fingertips before spreading out.

Logically, if more ridges are formed in a tight time frame, they should be closer to each other. If a bunch of lines meet grooves on another part of the pad, they can spiral, arc, and loop around each other.

It’s like what happens when multiple cross currents in the ocean collide, forcing the waves into intricate patterns. The timing, location, and angle of these ridges are highly sensitive to the local environment of the uterus.

“The confluence of patterned waves initiated at these variable locations determines the type of fingerprint pattern, which together with the inherent randomness of Turing systems provides an individual uniqueness for each fingerprint,” the authors write.

Subtle anatomical differences likely also play a role. Flexural folds, for example, seem to form boundaries along which ridges must flow, much like a rock in a river.

Later in fetal development, when mice and humans form sweat glands at the fingertips, our prints are differentiated even further.

The researchers say that all of these factors ultimately play into an intricate and dynamic system of development – ​​one that leads to the “endless variation in human fingerprint patterns” we see today.

The study was published in Cell.

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