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Archaeologists open a chamber sealed for 40,000 years, and what they find beneath the sand in Gibraltar changes what we thought we knew about Neanderthals: coastal hunters, glue makers, and Paleolithic artists

On the steep Mediterranean cliffs of Gibraltar, archaeologists have stepped into a room that no human had seen for tens of thousands of years. Hidden behind a plug of ancient sand in Vanguard Cave, part of the Gorham’s Cave Complex, a 13-meter chamber lay sealed for roughly 40,000 years, preserving rare clues to the final chapters of Neanderthal life on a changing coastline.

For scientists, this is not just a dramatic discovery. It is a time capsule that connects deep prehistory with very current questions about sea level rise, coastal ecosystems, and how humans respond when their environment transforms around them.

Gorham’s Cave Complex sits within the Gibraltar Nature Reserve and was inscribed as a UNESCO World Heritage Site in 2016, largely because it preserves some of the last known refuges of Neanderthals in Europe. Vanguard Cave and its neighbors show evidence of Neanderthal use for roughly 100,000 years, possibly until around 28,000 years ago, later than many other sites across the continent.

A ribosome-bound pseudoknot in the HCV coding region stimulates viral growth by tuning viral translation

Given that pk1 is located within the HCV coding region, we next investigated a potential role in translation elongation. We inserted pk1 into the ORF of Gaussia luciferase and used the HCV IRES to initiate translation (Figure 3 B, left). To ensure that the highly structured HCV IRES did not affect pk1 folding, we included a 99-nt linker sequence with low structural propensity between the HCV IRES and pk1. As controls, we used the pk1-unzip mutant and a randomized pk1, where the pk1 sequence was shuffled by three nucleotides, thereby maintaining the same amino acid composition as the WT pk1.

The RNA constructs described above were transfected into cells, and luciferase activity was measured at various time points to assess translation activity (Figure 3B, right). We observed that pk1 significantly inhibited translation elongation at all time points tested compared to the pk1-unzip and random controls. Notably, at 4 h post-transfection, there was nearly a 4-fold difference between the activity of pk1 and the pk1-unzip mutant, indicating that the pseudoknot structure itself, rather than just its constituent stems, is crucial for the observed translation inhibition (Figure 3B). To further examine the structural basis of this effect, we introduced a pk1-compensatory mutant that restores the disrupted base pairing in the pk1-unzip mutant using synonymous G-U wobble and A-U base pairs (sequence shown in Figure 3A).

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