No two fingerprints are exactly the same. That’s what makes them so useful for police and smartphones to positively identify people. Previous research has shown genes play a role in how the complex pattern of grooves and bumps on our fingertips form, so why don’t identical twins have identical fingerprints? A new study reveals that three families of signaling molecules—along with slight differences in the shape of the finger and the timing of skin growth—all interact to create our unique variations.
“It is a great example of how minor fluctuations … can generate endless variations in a pattern,” says Roel Nusse, a developmental biologist at Stanford Medicine who was not involved in the research.
The uneven surfaces of fingers improve grip and are found in humans and climbing species, such as koalas and chimpanzees. They also help us feel the difference between textures. Fingerprints form relatively early in fetal development, starting around the 13th week of gestation with the formation of indentations in the fingertips called primary ridges. These ridges develop into three main patterns: symmetrical, circular arrangements called “whorls”; longer, curved patterns called “loops”; and triangular ridges known as “arches.” Scientists have
identified several genes that influence which patterns end up in a person’s fingerprint, but the biochemical mechanisms that drive the formation of these ridges have proved elusive.
To shed light on this mystery, Denis Headon, a geneticist at the University of Edinburgh, and colleagues sequenced the RNA inside the nuclei of human embryonic fingertip cells to identify the genes being expressed during development. (The embryonic tissue came from people who terminated their pregnancies in the United Kingdom.) Those genes unearthed three different signaling pathways—families of proteins that carry instructions between cells—that each play a role in directing the growth of skin on the fingertips. Genes involved in two of these signaling pathways, known as WNT and BMP, are expressed in alternating stripes of cells in the developing fingertips, creating what will ultimately become the grooves and bumps of the fingerprint. A third factor, EDAR, is expressed alongside WNT in the developing grooves.
Mice also have simple ridge patterns on their digits. When researchers artificially suppressed the signaling pathways in mice, they found the WNT and BMP signals work in opposing ways. WNT appears to stimulate cell growth to create raised bumps in the outer layer of the skin, whereas BMP suppresses cell growth to form grooves. EDAR signals help determine the size and spacing of the ridges. For example, when researchers knocked out the WNT pathway, their digits formed no ridges at all, whereas knocking out the BMP pathway made the ridges wider. And in mice carrying a mutation that silenced EDAR activity, a polka dot pattern of ridges grew on their digits rather than stripes.
Ultimately, these
three signaling pathways work together to control the formation of primary ridges that grow into the corrugated structure of fingerprints, the team reports this week in Cell.
The opposing relationship between WNT and BMP in human fingertips is characteristic of Turing patterns—in which different, overlapping chemical activities give rise to complex patterns—which are widespread in nature and give rise to the
stripes and spots seen in animal fur and tropical fish skin. “The individual uniqueness [of fingerprints] comes from minute elements of the pattern,” Headon says, such as long ridges that stop, ridges that split in two, or short ridges called islands. “Turing patterns readily produce this type of fine-scale pattern,” he explains.
But the overall shape of the fingerprint pattern—whether the fingerprint ends up as a whorl, a loop, or an arch—depends on the anatomy of the finger and the exact timing of ridge formation. In the human embryonic tissues, the researchers found primary ridges start to form in up to three locations: the center of the fetal finger’s soft raised pad, the end of the finger under the nail, and the crease at the joint where the finger bends. From these three sites, the ridges spread out across the fingertip like “waves … each ridge serving to define the position of the next one out,” Headon says. The finger’s anatomy helps direct the pattern of finger cell growth. If the pads are large and symmetrical and ridges begin to form there early, they tend to produce a whorl. If the pads are longer and asymmetrical, they result in a loop. If ridges simply fail to form on the pad, or if they begin to form there late in development, then the ridges from the crease and the fingernail will meet in the middle, producing an arch.
The researchers also found that the same chemical signals—WNT, BMP, and EDAR—cause cells elsewhere in the body to develop into hair follicles. But our fingertips remain hair-free because the follicle formation on the palms of our hands halts early. This suggests different structures in the skin all start down the same early developmental path before diverging into specialized roles. “It may be that all of the structures formed by our largest organ, the skin—including hair, glands, fingerprints—are all fundamentally generated by the same mechanism,” Nusse says.
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