Caturday felids trifecta: kitten rescued after tornado; brave cat spooks bear; why cats can’t taste sweetness; and lagniappe

On May 9, the AP’s odd news site recounted a kitten rescue (click on screenshot to read):

An excerpt:

As storm chaser Ashton Lemley picked his way through a tornado-ravaged Mississippi trailer park, he heard the unmistakable meow of a kitten pierce the predawn darkness.

The homes were flattened just hours earlier as storms spawned at least three tornadoes across the bottom half of Mississippi, injuring a dozen at the trailer park in the rural community of Bogue Chitto.

Lemley had no idea where the kitten was, but he was determined to find it. After a few minutes, the meowing stopped, and Lemley feared the worst.

Then, five minutes later, he heard it again.

“I said, ‘Oh, he’s still alive!’” Lemley told The Associated Press on Thursday.

Lemley quickly dug under insulation from a flattened wall until his flashlight beam found the kitten — wet, scared and hiding between two wooden posts.

Lemley captured the moment on video: “Oh my goodness, I found him!” he says to the camera. “Are you OK? Come here – it’s OK. … We’ll get you cleaned up, baby. Don’t you worry.”

Lemley held the kitten in his arms for a few minutes before handing it off to the commander of the United Cajun Navy, a volunteer disaster-response group, who dried it off and took it to safety. Lemley marveled that it didn’t appear to be injured.“I’ve been in these situations so many times,” said Lemley, who has been chasing storms since 2010. “I don’t try to get overly emotional. But it is very heartbreaking to see any type of animal or human go through something like that.”

Lemley says there’s already a lot of interest from people who want to adopt the kitten if its owners are not located. Some, he said, want to name it Tornado.

It won’t be coming home with him, though: Lemley is allergic to cats.

Here’s a short video of the rescue. Look at that sodden little moggy! But it will be okay.

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From PetHelpful, we have a Tik Tok video and the video notes (indented below).

Little Bear Visits My Bedroom Window

An unexpected guest can make for a delightful surprise, and nothing illustrates this better than when I found a little black bear gazing curiously through my bedroom window. This moment was not only adorable but also a wonderful reminder of the beauty of wildlife right at our doorstep.

Bears are fascinating creatures known for their intelligence and curiosity. When a bear approaches residential areas, it often piques curiosity and concern among homeowners. Observing animals in their natural habitat can lead to valuable insights about their behavior. In this case, Little Bear seemed intrigued by what was happening inside the house, highlighting the need for a peaceful coexistence with wildlife..It’s important to remember that while these encounters can be entertaining, maintaining a safe distance from wild animals is essential for both human and animal safety. Living close to nature offers unique experiences, but it also requires responsibility. If you find yourself in a similar situation, enjoy the moment, take pictures if safe, but avoid feeding or trying to interact directly with wild animals.

In closing, this little bear visiting my window was a charming experience that reminded me of the vibrant wildlife that surrounds us. Have you had any wildlife encounters in your area? Share your stories or tips on safely observing animals in nature!

Here’s a very short video of the cat, safely inside, lashing out with its paw at the bear. Bear heads for the hills!

@missashleyrubes

I was reading in bed when I looked over to Little Bear looking into my window 🪟🐻 #bear #blackbear #animal #nature #wildlife

♬ Curious Animals – Eitan Epstein Music

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If you own a cat, you probably know that they can’t taste sweetness in food. This article from Space Daily (click on screenshot) explains why. Well, it’s not rocket science: cats don’t have the rcceptors to taste sweetness. Or rather, they have the genes that allowed their ancestors (and their living mammalian relatives) to taste sweetness, but the genes are broken. (This is, of course, proof of evolution: why else would a cat have genes that function in its relatives, but that are broken in felids?

An excerpt:

Cats are notoriously indifferent to sweet things. Pour syrup near a dog and the dog will investigate. Pour syrup near a cat and the cat will ignore it. Veterinarians and cat-food companies have long noted that cats show no preference for sugar in feeding tests, no matter how much sugar is presented. The reason is not a behavioural quirk or a learned aversion. It is genetic, and it traces back tens of millions of years to the point at which the ancestors of modern cats became obligate carnivores, eating only meat. The gene that produces a working sweet receptor on the tongue, called Tas1r2, has been broken in cats for so long that it no longer functions at all. A cat looking at a sugar cube is in the same sensory position as a human looking at an ultraviolet light source: the signal exists, but the receptor that would detect it does not.

The molecular discovery came in 2005 from a team led by Xia Li and Joseph Brand at the Monell Chemical Senses Center in Philadelphia, in collaboration with colleagues at the Waltham Centre for Pet Nutrition in the United Kingdom. Their paper in PLOS Genetics, titled “Pseudogenization of a Sweet-Receptor Gene Accounts for Cats’ Indifference toward Sugar,” established that the cat sweet receptor is not just inefficient. It is, at the genetic level, non-functional.

. . . The animals affected included the California sea lion, the southern fur seal, the Pacific harbor seal, the Asian small-clawed otter, the spotted hyena, the fossa (Madagascar’s largest carnivore), and the banded linsang. Crucially, the disabling mutations in each of these species occurred in different places within the Tas1r2 gene, indicating that the losses happened independently in each lineage, not via inheritance from a common ancestor. The same evolutionary pressure that turned off the gene in cats turned it off, separately, in at least seven other carnivorous lineages over the same broad timeframe. Behavioural testing of two of the genotyped species — the Asian small-clawed otter (broken Tas1r2) and the spectacled bear (intact Tas1r2, and predominantly herbivorous despite its order) — confirmed the pattern. The otter showed no preference for sweet compounds. The bear preferred sugars and even some non-caloric sweeteners.

. . . The animals affected included the California sea lion, the southern fur seal, the Pacific harbor seal, the Asian small-clawed otter, the spotted hyena, the fossa (Madagascar’s largest carnivore), and the banded linsang. Crucially, the disabling mutations in each of these species occurred in different places within the Tas1r2 gene, indicating that the losses happened independently in each lineage, not via inheritance from a common ancestor. The same evolutionary pressure that turned off the gene in cats turned it off, separately, in at least seven other carnivorous lineages over the same broad timeframe. Behavioural testing of two of the genotyped species — the Asian small-clawed otter (broken Tas1r2) and the spectacled bear (intact Tas1r2, and predominantly herbivorous despite its order) — confirmed the pattern. The otter showed no preference for sweet compounds. The bear preferred sugars and even some non-caloric sweeteners.

And since people here should know some science, you’ll be able to understand this from the paper’s abstract:

Because the mammalian sweet-taste receptor is formed by the dimerization of two proteins (T1R2 and T1R3; gene symbols Tas1r2 and Tas1r3), we identified and sequenced both genes in the cat by screening a feline genomic BAC library and by performing PCR with degenerate primers on cat genomic DNA. Gene expression was assessed by RT-PCR of taste tissue, in situ hybridization, and immunohistochemistry. The cat Tas1r3 gene shows high sequence similarity with functional Tas1r3 genes of other species. Message from Tas1r3 was detected by RT-PCR of taste tissue. In situ hybridization and immunohistochemical studies demonstrate that Tas1r3 is expressed, as expected, in taste buds. However, the cat Tas1r2 gene shows a 247-base pair microdeletion in exon 3 and stop codons in exons 4 and 6. There was no evidence of detectable mRNA from cat Tas1r2 by RT-PCR or in situ hybridization, and no evidence of protein expression by immunohistochemistry. Tas1r2 in tiger and cheetah and in six healthy adult domestic cats all show the similar deletion and stop codons. We conclude that cat Tas1r3 is an apparently functional and expressed receptor but that cat Tas1r2 is an unexpressed pseudogene. A functional sweet-taste receptor heteromer cannot form, and thus the cat lacks the receptor likely necessary for detection of sweet stimuli. This molecular change was very likely an important event in the evolution of the cat’s carnivorous behavior.

The upshot: tasting sweetness in mammals requires a protein that is a dimer made from the product of two genes. In house cats (and some other carnivores), one of the genes is expressed normally but the other is nonfunctional because of a large deletion of the DNA sequence, so that the dimer itself isn’t formed. Ergo cats can’t detect sweetness, and thus you shouldn’t expect your cats to like sweets (they shouldn’t get them anyway). If your cat licks ice cream, it is tasting not the sweetness but the dairy-ness: fats and proteins.  Cheetahs and tigers also lack the dimeric protein.

Why do dogs taste sweetness and cats don’t? Because dogs produce the dimer and cats don’t.  Somewhere in the ancestor of all felids, the gene for Tastr2 experienced a deletion.  Because all cats are obligate carnivores, and don’t eat stuff like berries, they have no “need” to taste sweetness, so a deleted gene is not a deleterious gene. It just continued to mutate, staying in the DNA but doing nothing.

I suppose d*g ancestors, and mammals like bears and hedgehogs, do benefit from sugar in their diet and so have retained the genes to detect it. (We do, too: sugars were valuable components of the diet in us and our primate relatives, and so our taste chemistry evolved to not only detect sweetness, but also find it pleasurable so that we seek out a needed nutrient. Unfortunately, sugars are much more common now than in the millions of years of our ancestry since we diverged from the chimp/bonobo lineage; and so we eat too many of them and get cavities and grow obese.)

The alternative theory is that God decided to make cats obligate meat-eaters, and so he left out their ability to detect sugar. But that doesn’t work because why would God give cats genes that are very similar to those of their sweetness-tasting relatives, but don’t work?  The creation-by-God theory fails, and we’re left only with common ancestry, i.e., evolution.

We have a similar broken gene, as I describe in Why Evolution is True:

The most famous human pseudogene is GLO, so called because in other species it produces an enzyme called L-gulono-γ-lactone oxidase. This enzyme is used in making vitamin C (ascorbic acid) from the simple sugar glucose. Vitamin C is essential for proper metabolism, and virtually all mammals have the pathway to make it—all, that is, except for primates, fruit bats, and guinea pigs. In these species, vitamin C is obtained directly from their food, and normal diets usually have enough. If we don’t ingest enough vitamin C, we get sick: scurvy was common among fruit-deprived seamen of the nineteenth century.

The reason why primates and these few other mammals don’t make their own vitamin C is because they don’t need to. Yet DNA sequencing tells us that primates still carry most of the genetic information needed to make the vitamin.

It turns out that the pathway for making vitamin C from glucose involves a sequence of four steps, each promoted by the product of a different gene. Primates and guinea pigs still have active genes for the first three steps, but the last step, which requires the GLO enzyme, doesn’t take place: GLO has been inactivated by a mutation. It has become a pseudogene, called ¯ψGLO” (ψ is the Greek letter psi, standing for “pseudo”). ψGLO doesn’t work because a single nucleotide in the gene’s DNA sequence is missing. And it’s exactly the same nucleotide that is missing in other primates. This shows that the mutation that destroyed our ability to make vitamin C was present in the ancestor of all primates, and was passed on to its descendants. The inactivation of GLO in guinea pigs happened independently, since it involves different mutations. It’s highly likely that since fruit bats, guinea pigs, and primates got plenty of vitamin C in their diet, there was no penalty for inactivating the pathway that made it. This could even have been beneficial since it eliminated a protein that might have been costly to produce.

A dead gene in one species that is active in its relatives is evidence for evolution, but there’s more. When you look at ψGLO in living primates, you find out that its sequence is more similar between close relatives than between more distant ones. The sequences of human and chimp ψGLO, for example, resemble each other closely, but differ more from the ψGLO of orangutans, which are more distant relatives. What’s more, the sequence of guinea pig ψGLO is very different from that of all primates.

Only evolution and common ancestry can explain these facts.

Inactive pseudogenes that are functional in relatives constitute some of the strongest evidence for evolution, as there is no alternative theory that explains them. The article above alludes to the gene loss being a product of evolution, but doesn’t mention something that I see as crucial given Americans’ reluctance to accept evolution: the nature of the gene loss and the sequence similarity among pseudogenes is strong evidence for evolution.

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Lagniappe:  From an Archaeology and Art Facebook post:  Draw a cat using only straight lines.  Here you go:

And extra lagniappe (is that redundant?). Only in Turkey will there be spectators!

🇹🇷 A stray cat in Turkey shows up every morning to hug the man who fed her.

Not sometimes. Every single day.

His shop is now packed with people who come just to watch.pic.twitter.com/TUVI9NPq7n

— Mario Nawfal (@MarioNawfal) May 18, 2026

h/t: Ginger K.,