Approximately 35 % of the mouse genes are indispensable for life, thus, global knock-out (KO) of those genes may result in embryonic or early postnatal lethality due to developmental abnormalities. Several KO mouse lines are valuable human disease models, but viable homozygous mutant mice are frequently required to mirror most symptoms of a human disease. The site-specific gene editing systems, the transcription activator-like effector nucleases (TALENs), Zinc-finger nucleases (ZFNs) and the clustered regularly interspaced short palindrome repeat-associated Cas9 nuclease (CRISPR/Cas9) made the generation of KO mice more efficient than before, but the homozygous lethality is still an undesired side-effect in case of many genes. The literature search was conducted using PubMed and Web of Science databases until June 30th, 2020. The following terms were combined to find relevant studies: “lethality”, “mice”, “knock-out”, “deficient”, “embryonic”, “perinatal”, “rescue”. Additional manual search was also performed to find the related human diseases in the Online Mendelian Inheritance in Man (OMIM) database and to check the citations of the selected studies for rescuing methods. In this review, the possible solutions for rescuing human disease-relevant homozygous KO mice lethal phenotypes were summarized.

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Numtogenesis is the phenomenon of mitochondrial sequence localisation and integration into the nuclear genome. This is an ongoing process which contributed to the complexity of eukaryotic genomes. The sequences that are integrated into the nuclear genome are called nuclear mitochondrial sequences (numt). numts have a wide variety of applications in tumor biology, phylogenetic studies, forensic research and so on. Mus musculus musculus is the most popular model organism. Numerous mouse strains are used in medical research to model human diseases. numts were described in the genome of Mus musculus musculus just like in many other species however the characterisation of numts in different mouse strains is missing. In this study we explored the patterns of numtogenesis in 16 mouse strains by aligning the nuclear genomes with the corresponding mitochondria. Investigation of numts shed light on strain specific differences and resembles the phylogenetic relationships as to our current knowledge in most of the cases.

Green fluorescent protein (GFP) transgenic laboratory animals (mice, rats, rabbits etc.) are commonly used in basic research for modelling human diseases, studying organ development, cell transfer during pregnancy or tissue engineering. The expression of the fluorescent protein can be either ubiquitous or tissue-specific, depending on the transgenic construct and the integration site of the transgene. Despite the wide applications, the data about the physiological parameters of GFP transgenic animals are limited. In most of the transgenic lines, GFP does not induce any detrimental effect, but GFP-induced conditions are also reported. Altered T-lymphopoiesis and low white blood cell (WBC) count were observed in human ubiquitin C promoter-driven GFP transgenic (UBC-GFP) mice due to latent stem cell defect. The aim of the present study was to examine the effects of the Venus fluorescent protein on hematopoiesisand general health of transgenic rabbits, thus, hematology along with selected serum parameters were measured.