The main number of genome editing events in plant objects obtained during the last decade with the help of specific nucleases zinc finger (ZFN), transcription activator-like effector nucleases (TALEN), and clustered regularly interspaced short palindromic repeats (CRISPR)/Cas are the microindels causing frameshift and subsequent gene knock-out. The knock-ins of genes or their parts, i.e., the insertion of them into a target genome region, are between one and two orders of magnitude less frequent. First and foremost, this is associated with the specific features of the repair systems of higher eukaryotes and the availability of the donor template in accessible proximity during double-strand break (DSB) repair. This review briefs the main repair pathways in plants according to the aspect of their involvement in genome editing. The main methods for increasing the frequency of knock-ins are summarized both along the homologous recombination pathway and non-homologous end joining, which can be used for plant objects.

Most the pharmaceutical proteins are derived not from their natural sources, rather their recombinant analogs are synthesized in various expression systems. Plant expression systems, unlike mammalian...

Chemical mutagenesis of the pea laboratory line SGE with ethyl methane sulfonate was carried out. In the analysis of 425 families (2069 plants) of the M₂ generation 45 putative symbiotic mutants were selected, including 30 mutants that form ineffective nodules (the Fix⁻ phenotype), 13 mutants that are unable to form nodules (the Nod⁻ phenotype) and two mutants that form occasional nodules (the Nod^+/− phenotype). For one Nod⁻ and five Fix⁻ mutants monogenic inheritance and recessive phenotype manifestation were shown. For the Fix⁻ mutant SGEFix⁻-9 the presence of an additional mutation that leads to the Nod^+/− phenotype was shown. Complementation analysis showed that the mutant phenotype of the line SGEFix⁻-5 is determined by a mutation in the sym33 gene; of the line SGEFix⁻-6, in the sym40 gene; of the line SGEFix⁻-7, in the sym27 gene; and of the line SGEFix⁻-8, in the sym25 gene.