Fingerprints: Development and use.
The genetic basis of fingerprints.
Fingerprints are ridges that are found on the epidermal layer of the skin which is at the surface of the fingers. They are present on most of the people except a few individuals who have rare genetic conditions such as Naegeli-Franceschetti-Jadassohn syndrome (NFJS), Dermatopathia pigmentosa reticularis (DPR) and Adermatoglyphia. Two fundamental principles of fingerprint identification are that fingerprints are permanent and unique, fingerprints never change and no two fingerprints are the same. Their main function of the body is to enhance the sense of touch as well as provide good grip on smooth objects. They grow larger throughout a person’s life however their basic structure remains constant. They can be temporarily obscured when the skin is damaged; but once healed, the ridges grow back in the exact same pattern. (Nousbeck, J. Et al (2014).
The genetic background of fingerprints is not clearly known, however genes that either code for them or that code for events that leads to their formation largely depend on the environment that where present during their formation. As with other genes the phenotypic expression of fingerprints is largely affect by external conditions. In the third and fourth months of gestation the skin of a foetus transforms from thin transparency to a waxy coating. During this time the middle layer of skin, called the basal layer, begins to outgrow the inner dermis and epidermis skin layers. The buckling and folding of this skin layer is partially responsible for the unique stresses in fingertip pads that become visible as fingerprints.
Ridges are the faint lines on the fingertips that create the foundation of a fingerprint. A foetus touches surrounding structures its position in the womb and the density of the womb’s amniotic fluid determine how every individual ridge will form. The level of activity of a foetus and the general chaos of the conditions of the womb prevent fingerprints from developing the same way in foetuses. By the time a foetus is six months old its fingerprints are fully developed. The ridges on a foetus’s fingertips have formed three main patterns by this time, categorized as arches, loops and whorls, with numerous patterns in between.
People with Adermatoglyphia have a mutation in a region of DNA that codes for a protein called SMARCAD1, while people with fingerprints have a normal form of the gene. The shorter, mutated version of the gene, they found, interferes with the way RNA is spliced together which is a crucial step in the process of using a gene to produce a protein, which prevents the protein from forming correctly. No further studies done so far have proved how this protein affects fingerprints, therefor it could be concluded that the presence of fingerprints is dependent on the gene coding for this protein. This is so because its absence causes the latter condition. (Nousbeck, J. Et al (2014).
The reasons why fingerprints are different in every person is that even though twins may have the same DNA each of them touched and moved differently from the other to add on each of them experienced different amniotic fluid pressure due to their positions. Crossing over during meiosis also contributes to this difference because of random assortment of chromosomes. This ultimately differentiates how the orientation of the contours or ridges of the epidermal layer are laid out.
References
Nousbeck, J. Et al (2014). Mutations in SMARCAD1 cause autosomal dominant adermatoglyphia and perturb the expression of epidermal differentiation-associated genes. Brit. J. Derm. 171: 1521-1524,. [PubMed: 24909267
http://www.omim.org/entry/136000
