RESUMEN
Black phosphorus (BP) is a layered semiconductor with outstanding properties, making it a promising candidate for optoelectronic and other applications. BP synthesis is an intriguing task largely due to the insufficient understanding of the synthesis mechanism. In this work, we use density functional theory calculations to examine BP and its precursor red phosphorus as they are formed from P4 building blocks. Our results suggest that, without external effects such as pressure or addition of a catalyst, the precursor is energetically favored in the initial steps of the synthesis, even though BP is the more stable allotrope. The higher energy of BP is dictated by its 2D geometry that gives rise to the higher number of high-energy strained bonds at the edge compared to the 1D geometry of red phosphorus. The elucidated BP formation pathway provides a natural explanation for the effectiveness of the recently discovered Sn/I catalyst used in BP synthesis.
RESUMEN
Translesion DNA synthesis (TLS) is a DNA damage tolerance mechanism carried out by low-fidelity DNA polymerases that bypass DNA lesions, which overcomes replication stalling. Despite the miscoding nature of most common DNA lesions, several of them are bypassed in mammalian cells in a relatively accurate manner, which plays a key role maintaining a low mutation load. Whereas it is generally agreed that TLS across the major UV and sunlight induced DNA lesion, the cyclobutane pyrimidine dimer (CPD), is accurate, there were conflicting reports on whether the same is true for the thymine-thymine pyrimidine-pyrimidone(6-4) ultraviolet light photoproduct (TT6-4PP), which represents the second most common class of UV lesions. Using a TLS assay system based on gapped plasmids carrying site-specific TT6-4PP lesions in defined sequence contexts we show that the DNA sequence context markedly affected both the extent and accuracy of TLS. The sequence exhibiting higher TLS exhibited also higher error-frequency, caused primarily by semi-targeted mutations, at the nearest nucleotides flanking the lesion. Our results resolve the discrepancy reported on TLS across TT6-4PP, and suggest that TLS is more accurate in human cells than in mouse cells.