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How many of you have scanned your fingerprints? I am sure most of you have done that at least once in your life. These swirly creases are unique markers for each human inhabiting planet earth. Well, not everyone but most of us. Imagine you are running behind on your schedule and have to attend an important class, but the school has a biometric system for identification to allow entry. You run over to the scanner, slam your finger, and nothing happens. You lift your finger to rescan. Again, nothing happens. Your day worsens with each passing minute, insurmountable frustration weighing down on your shoulders. It is an issue faced daily by individuals who lack fingerprints. Those born without these lines face the veritable challenge of identification in many walks of life. But, if every embryo is subjected to the same development process during the gestation period, how do some individuals not possess this unique identity marker?
The answer to this lies in our genes. But first, let us dive deep into these patterns. Typically, unique fingerprints develop during pregnancy, also called the gestation period. This medley of tiny grooves, swirls and arches, known as dermatoglyphs, is the world's most collected biometric data and is distinct for every person. We use them everywhere, from biometric attendance to opening our smartphone lock screens. However, a few individuals have been born without fingerprints. The condition is called adermatoglyphia. In simple terms, these individuals' finger pads, toes, palms, and soles are smooth, with just a little bit of creasing and lack dermatoglyphs.
Adermatoglyphia is caused by a mutation in the SMARCAD1 gene, responsible for the development of fingerprints. This gene encodes two versions of SMARCAD1 protein: the full-length version is expressed in multiple tissues, and the shorter version is expressed only in the skin. The full-length SMARCAD1 protein is involved in regulating the activity of various genes responsible for maintaining the stability of genetic information in cells. Not much is known about the function of the skin-specific version, but it appears to play a crucial role in dermatoglyph formation.
The SMARCAD1 gene mutation that leads to adermatoglyphia affects only the skin-specific version of the SMARCAD1 protein. The shorter, mutated version of the gene impedes how RNA is spliced together, preventing the protein from forming correctly.
These mutations reduce the amount of SMARCAD1 protein available in skin cells. Although the mechanism of how these genetic changes cause adermatoglyphia is not clear, it is speculated that a shortage of the SMARCAD1 protein impairs signalling pathways required for normal skin development, including the formation of dermatoglyphs. In addition, it is inherited in an autosomal dominant manner. Therefore, a single copy of the mutated SMARCAD1 gene in each cell is sufficient to lead to adermatoglyphia. In most cases, individuals have one parent who suffers from the condition.
Also known as 'Immigration delay disease', the condition poses severe tribulations to individuals migrating or even looking for a job in fields that utilise fingerprints for identifying individuals. Securing employment is a massive issue for such people, but besides identification problems, the only serious physical symptom is less than a normal number of sweat glands. Due to the inability to sweat properly, these individuals have a high chance of suffering from heat strokes. On the flipside, such individuals do not have to worry about identity theft through biometric identification (just saying). Though I would never condone crime, an individual with this mutation can easily get away with anything and not be traced. Other genetic disorders like dermatopathia pigmentosa reticularis also lead to missing fingerprints, but they also cause severe health issues such as brittle teeth and thin hair.
Conditions like adermatoglyphia have opened the doors to a new world for researchers who continue to find novel ways to understand the complex human body. For instance, if it were not for adermatoglyphia, we would have never known the role of the SMARCAD1 gene in skin formation. There is a lot about the human body that we still do not know, and a lot of what we have found is because of mutations, and the quest to understand every aspect of the intricate and inexplicable human body continues.
References:
1. Sarfraz, N. (2019). Adermatoglyphia: Barriers to Biometric Identification and the Need for a Standardized Alternative. Cureus. doi: 10.7759/cureus.4040
2. Nousbeck, J., Sarig, O., Magal, L., Warshauer, E., Burger, B., Itin, P., & Sprecher, E. (2014). Mutations inSMARCAD1cause autosomal dominant adermatoglyphia and perturb the expression of epidermal differentiation-associated genes. British Journal Of Dermatology, 171(6), 1521-1524. doi: 10.1111/bjd.13176Top of Form
3. Magazine, S., & Stromberg, J. (2014). Adermatoglyphia: The Genetic Disorder Of People Born Without Fingerprints. Retrieved 26 February 2022, from https://www.smithsonianmag.com/science-nature/adermatoglyphia-genetic-disorder-people-born-without-fingerprints-180949338/
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4. Burger, B., Fuchs, D., Sprecher, E., & Itin, P. (2011). The immigration delay disease: Adermatoglyphia–inherited absence of epidermal ridges. Journal Of The American Academy Of Dermatology, 64(5), 974-980. doi: 10.1016/j.jaad.2009.11.013
5. Burger, B., Fuchs, D., Sprecher, E., & Itin, P. (2011). The immigration delay disease: Adermatoglyphia–inherited absence of epidermal ridges. Journal Of The American Academy Of Dermatology, 64(5), 974-980. doi: 10.1016/j.jaad.2009.11.013
About the Author
Author: Himanshi Yadav
Bio: Himanshi Yadav has recently completed Masters in Zoology with a specialization in Molecular Endocrinology and Reproduction from Miranda House, University of Delhi. She aspires to research and delve deep into Neuroscience and Cancer Biology. Her other fields of interest include Public health. She is keen on broadening the horizons of how science is being communicated and actively advocates for gender equality in STEM, inclusivity, and mental health awareness.
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