Gene expression for youthful skin

Some individuals' skin appears more youthful than their chronologic age. Although many people try to achieve this with creams, lotions, injections, and surgeries, new research indicates that increased expression of certain genes may be the key to intrinsically younger looking and younger behaving skin. It's not just the genes you are born with, but which ones turn on and off over time,wide range of processes in the skin affected by aging, and specific gene expression patterns in women who appear younger than their chronologic age.

Reseachers collected and integrated data at the molecular, cellular, and tissue levels from the sun-exposed skin (face and forearm) and sun-protected skin (buttocks) of  white women between 20 to 70 years. As part of the study, the team looked for gene expression patterns common in women who appeared years younger than their chronologic age.The physical appearance of facial skin was captured through digital images and analysis. Skin samples were processed for analysis and saliva samples were collected for genotyping.

The analyses revealed progressive changes from the 20s to the 70s in pathways related to oxidative stress , energy metabolism, senescence (aging) and skin barrier. These changes were accelerated in the 60s and 70s. Comparing sun-exposed and sun-protected skin samples revealed that certain genetic changes are likely due to photoaging. The gene expression patterns from the women in the study who were younger appearing were similar to those in women who were actually younger in age. These women had increased activity in genes associated with basic biologic processes, including DNA repair, cell replication, response to oxidative stress, and protein metabolism.

Women with exceptionally youthful-appearing facial skin in older age groups also had higher expression of genes associated with mitochondrial structure and metabolism, overall epidermal structure, and barrier function in their facial epidermal samples, as well as dermal matrix production.A better understanding of the genes associated with youthful-appearing skin may point to new strategies to enhance factors that slow the skin's aging process. This work also confirmed that ultraviolent (UV) exposure is a main driver and accelerator of skin aging.
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RNA modification and brain development

A chemical tag added to RNA during embryonic development regulates how the early brain grows, when this development goes wrong, it may cause psychiatric disorders in people. Researchers used animal models and mini-brains, made from human stem cells to relate their findings to conditions found in people.

Researchers have discovered chemical modifications to messenger RNA mRNA across the genome at certain sites and found that these changes are dynamic- a specific chemical group is added and taken off by enzymes in a regular, pattern. The chemical group studied in the Cell paper, m6A, is the most prevalent modification to mRNA in human cells.

The current thinking is that a tightly controlled molecular process guides the complicated development of the brain before birth and the process relies on a precise sequence of genes being turned on and off. However, even subtle mistakes in this process can become serious issue. The classic view of this control is that DNA codes for RNA, guiding which proteins will be made by cells. However, mRNA can be modified along the way so that it can produce proteins with many variations.

A new field called epitranscriptomics was discovered during the research. The Cell paper is the first study of epitranscriptomics in the embryonic mammalian brain, and the key is m6A, a marker for molecules bound for disposal within the cell. Normally, m6A-tagged mRNAs are related to such processes as cell replication and neuron differentiation, and m6A-tagging promotes their decay after they are no longer needed.

If m6A is not added on the correct time schedule to a garbage-bound molecule, the developmental train goes down the wrong tracks because developing brain cells get stuck at an earlier stage because the m6A cues for taking out the cellular trash are misread or not read at all. The researchers found that in a mouse model with depleted m6A, cell replication is prolonged, so that stem-cell differentiation, which normally reels out daughter cells in an orderly fashion, gets stuck. The knockout mouse develops less brain cells such as neurons and glia cells, and therefore has abnormal circuitry and a non-functioning brain.

Neuron development in the mini-brains that was developed is similar to what happens in people, modeling fetal brain development up to the second trimester. Human stem cells had a greater number of m6A tags compared to mouse cells. Many of the genes associated with genetic risk for certain conditions, such as schizophrenia and autism spectrum disorder, are only m6A-tagged in humans, not in mice, raising the possibility that dysregulation at this level of gene expression may contribute to certain human brain disorders.
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