Endoreplication-Why Are We Not Using Its Full Application Potential?

Endoreplication-a process that is common in plants and also accompanies changes in the development of animal organisms-has been seen from a new perspective in recent years. In the paper, we not only shed light on this view, but we would also like to promote an understanding of the application potential of this phenomenon in plant cultivation. Endoreplication is a pathway for cell development, slightly different from the classical somatic cell cycle, which ends with mitosis. Since many rounds of DNA synthesis take place within its course, endoreplication is a kind of evolutionary compensation for the relatively small amount of genetic material that plants possess. It allows for its multiplication and active use through transcription and translation. The presence of endoreplication in plants has many positive consequences. In this case, repeatedly produced copies of genes, through the corresponding transcripts, help the plant acquire the favorable properties for which proteins are responsible directly or indirectly. These include features that are desirable in terms of cultivation and marketing: a greater saturation of fruit and flower colors, a stronger aroma, a sweeter fruit taste, an accumulation of nutrients, an increased resistance to biotic and abiotic stress, superior tolerance to adverse environmental conditions, and faster organ growth (and consequently the faster growth of the whole plant and its biomass). The two last features are related to the nuclear-cytoplasmic ratio-the greater the content of DNA in the nucleus, the higher the volume of cytoplasm, and thus the larger the cell size. Endoreplication not only allows cells to reach larger sizes but also to save the materials used to build organelles, which are then passed on to daughter cells after division, thus ending the classic cell cycle. However, the content of genetic material in the cell nucleus determines the number of corresponding organelles. The article also draws attention to the potential practical applications of the phenomenon and the factors currently limiting its use.

Mitochondrial transcription factor A is the major protein in rodent hepatocytes that recognizes DNA lesions induced by N-acetoxy-acetylaminofluorene.

Extracts from rodent liver cells contain an abundant protein that recognizes DNA adducts induced by the chemical carcinogen N-acetoxy-acetylaminofluorene (AAAF). This protein also has a strong affinity for DNA damaged by cisplatin (DDP), but not by benzo(a)pyrene diolepoxide or UV-radiation, and has been termed AAAF/DDP-DDB. Here we purified this protein from rat tissue and analyzed it by mass spectrometry and identified it as mitochondrial transcription factor A (TFAM). Experiments with bacterially expressed recombinant TFAM confirmed its high affinity for DNA damaged by AAAF. Assuming its abundance and specificity for AAAF induced lesions, TFAM may significantly impede recognition and repair of DNA adducts induced by AAAF and other derivatives of 2-aminofluorene.