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Why Do We Tan?

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Sit out in the sun too long and ultraviolet radiation from sunlight penetrates your skin and cells, damaging their RNA and DNA. This is bad news, as DNA provides our bodies with all the genetic instructions they need to develop, survive and go about their business, and this kind of DNA damage can lead to skin cancer. To protect you from this, your body helpfully tans, darkening the the skin with a pigment called melanin that reduces UV penetration into cells.

UV radiation stimulates the darkening of existing melanin and spurs increased melanogenesis, the production of new melanin. Cells called melanocytes generate the pigment and push it out of the cell, where it darkens the skin and absorbs and transforms absorbed UV energy into heat.

Melanogenesis results in a delayed tan that only becomes visible several hours after UV exposure and lasts longer than the tanning caused by darkening of existing melanin. Over time, a tan fades as darkened skin layers are pushed upward by new cells with less melanin, and are eventually scaled off.

Why do we get sunburn?

While we might say someone with sunburn was out “baking” too long or got “fried,” sunburns are different from the burn one might get from, say, touching a hot stove. That’s a thermal burn caused by the heat of the stove. While the sun does give off heat, a sunburn is caused by ultraviolet-B radiation.

When someone’s exposure to UV radiation exceeds their body’s ability to protect the skin with tanning, the radiation  causes damage to DNA, like we talked about above. This prompts the body to try and fix things. Bloodflow to the capillary bed of the dermis (the second outermost layer of skin) increases so cells can repair the damage, which results in warmth and redness of the skin. Inflammatory immune cells also flock to the damaged tissue, causing us to perceive pain and, hopefully, consider staying out of the sun for a while. Eventually, the damaged skin cells die, and the burned skin starts to peel.

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Big Questions
How Are Speed Limits Set?
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When driving down a road where speed limits are oppressively low, or high enough to let drivers get away with reckless behavior, it's easy to blame the government for getting it wrong. But you and your fellow drivers play a bigger a role in determining speed limits than you might think.

Before cities can come up with speed limit figures, they first need to look at how fast motorists drive down certain roads when there are no limitations. According to The Sacramento Bee, officials conduct speed surveys on two types of roads: arterial roads (typically four-lane highways) and collector streets (two-lane roads connecting residential areas to arterials). Once the data has been collected, they toss out the fastest 15 percent of drivers. The thinking is that this group is probably going faster than what's safe and isn't representative of the average driver. The sweet spot, according to the state, is the 85th percentile: Drivers in this group are thought to occupy the Goldilocks zone of safety and efficiency.

Officials use whatever speed falls in the 85th percentile to set limits for that street, but they do have some wiggle room. If the average speed is 33 mph, for example, they’d normally round up to 35 or down to 30 to reach the nearest 5-mph increment. Whether they decide to make the number higher or lower depends on other information they know about that area. If there’s a risky turn, they might decide to round down and keep drivers on the slow side.

A road’s crash rate also comes into play: If the number of collisions per million miles traveled for that stretch of road is higher than average, officials might lower the speed limit regardless of the 85th percentile rule. Roads that have a history of accidents might also warrant a special signal or sign to reinforce the new speed limit.

For other types of roads, setting speed limits is more of a cut-and-dry process. Streets that run through school zones, business districts, and residential areas are all assigned standard speed limits that are much lower than what drivers might hit if given free rein.

Have you got a Big Question you'd like us to answer? If so, let us know by emailing us at bigquestions@mentalfloss.com.

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Big Questions
Do Bacteria Have Bacteria?
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Drew Smith:

Do bacteria have bacteria? Yes.

We know that bacteria range in size from 0.2 micrometers to nearly one millimeter. That’s more than a thousand-fold difference, easily enough to accommodate a small bacterium inside a larger one.

Nothing forbids bacteria from invading other bacteria, and in biology, that which is not forbidden is inevitable.

We have at least one example: Like many mealybugs, Planococcus citri has a bacterial endosymbiont, in this case the β-proteobacterium Tremblaya princeps. And this endosymbiont in turn has the γ-proteobacterium Moranella endobia living inside it. See for yourself:

Fluorescent In-Situ Hybridization confirming that intrabacterial symbionts reside inside Tremblaya cells in (A) M. hirsutus and (B) P. marginatus mealybugs. Tremblaya cells are in green, and γ-proteobacterial symbionts are in red. (Scale bar: 10 μm.)
Fluorescent In-Situ Hybridization confirming that intrabacterial symbionts reside inside Tremblaya cells in (A) M. hirsutus and (B) P. marginatus mealybugs. Tremblaya cells are in green, and γ-proteobacterial symbionts are in red. (Scale bar: 10 μm.)

I don’t know of examples of free-living bacteria hosting other bacteria within them, but that reflects either my ignorance or the likelihood that we haven’t looked hard enough for them. I’m sure they are out there.

Most (not all) scientists studying the origin of eukaryotic cells believe that they are descended from Archaea.

All scientists accept that the mitochondria which live inside eukaryotic cells are descendants of invasive alpha-proteobacteria. What’s not clear is whether archeal cells became eukaryotic in nature—that is, acquired internal membranes and transport systems—before or after acquiring mitochondria. The two scenarios can be sketched out like this:


The two hypotheses on the origin of eukaryotes:

(A) Archaezoan hypothesis.

(B) Symbiotic hypothesis.

The shapes within the eukaryotic cell denote the nucleus, the endomembrane system, and the cytoskeleton. The irregular gray shape denotes a putative wall-less archaeon that could have been the host of the alpha-proteobacterial endosymbiont, whereas the oblong red shape denotes a typical archaeon with a cell wall. A: archaea; B: bacteria; E: eukaryote; LUCA: last universal common ancestor of cellular life forms; LECA: last eukaryotic common ancestor; E-arch: putative archaezoan (primitive amitochondrial eukaryote); E-mit: primitive mitochondrial eukaryote; alpha:alpha-proteobacterium, ancestor of the mitochondrion.

The Archaezoan hypothesis has been given a bit of a boost by the discovery of Lokiarcheota. This complex Archaean has genes for phagocytosis, intracellular membrane formation and intracellular transport and signaling—hallmark activities of eukaryotic cells. The Lokiarcheotan genes are clearly related to eukaryotic genes, indicating a common origin.

Bacteria-within-bacteria is not only not a crazy idea, it probably accounts for the origin of Eucarya, and thus our own species.

We don’t know how common this arrangement is—we mostly study bacteria these days by sequencing their DNA. This is great for detecting uncultivatable species (which are 99 percent of them), but doesn’t tell us whether they are free-living or are some kind of symbiont. For that, someone would have to spend a lot of time prepping environmental samples for close examination by microscopic methods, a tedious project indeed. But one well worth doing, as it may shed more light on the history of life—which is often a history of conflict turned to cooperation. That’s a story which never gets old or stale.

This post originally appeared on Quora. Click here to view.

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