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| 1 | Gene redundancy and gene compensation:An updated view显示文摘Gene knockdown approaches using antisense oligo nucleotides or analogs such as siRNAs and morpholinos have been widely adopted to study gene functions although the off-target issue has been always a concern in these studies.On the other hand,classic genetic analysis relies on the availability of loss-offunction or gain-of-function mutants.The fast development of genome editing technologies such as TALEN and CRISPR/Cas9 has greatly facilitated the generation of null mutants for the functional studies of target genes in a variety of organisms such as zebrafish.Surprisingly,an unexpected discrepancy was observed between morphant phenotype and mutant phenotype for many genes in zebrafish,i.e.,while the morphant often displays an obvious phenotype,the corresponding null mutant appears relatively normal or only exhibits a mild phenotype due to gene compensation.Two recent reports have partially answered this intriguing question by showing that a pre-mature termination codon and homologous sequence are required to elicit the gene compensation and the histone modifying complex COMPASS is involved in activating the expression of the compensatory genes.Here,I summarize these exciting new progress and try to redefine the concept of genetic compensation and gene compensation. | Jinrong Peng | 2019 | Journal of Genetics and Genomics2019，46，7： | 4 |
| 2 | Induction of clusterin Expression by Neuronal Cell Death in Zebrafish显示文摘Clusterin,a protein associated with multiple functions,is expressed in a wide variety of mammalian tissues.Although clusterin is known to be involved in neurodegenerative diseases,ageing,and tumorigenesis,a detailed analysis of the consequences of gain- or loss-offunction approaches has yet to be performed to understand the underlying mechanisms of clusterin functions.Since clusterin levels change in neurological diseases,it is likely that clusterin contributes to cell death and degeneration in general.Zebrafish was investigated as a model system to study human diseases.During development,zebrafish clusterin was expressed in the notochord and nervous system.Embryonic overexpression of clusterin by mRNA microinjection did not affect axis formation,whereas its knock-down by anti-sense morpholino treatment resulted in neuronal cell death.To analyze the function of clusterin in neurodegeneration,a transgenic zebrafish was investigated,in which nitroreductase expression is regulated under the control of a neuron-specific huC promoter which is active between the stages of early neuronal precursors and mature neurons.Nitroreductase turns metronidazole into a cytotoxic agent that induces cell death within 12 h.After metronidazole treatment,transgenic zebrafish showed neuron-specific cell death.Interestingly,we also observed a dramatic induction of clusterin expression in the brain and spinal cord in these fish,suggesting a direct or indirect role of clusterin in neuronal cell death and thus,more generally,in neurodegeneration. | Yun-Mi Jeong Tae-Eun Jin Jung-Hwa Choi Mi-Sun Lee Hyun-Taek Kim Kyu-Seok Hwang Doo-Sang Park Hyun-Woo Oh Joong-Kook Choi Vladimir Korzh Melitta Schachner Kwan-Hee You Cheol-Hee Kim | 2014 | Journal of Genetics and Genomics2014，41，11： | 0 |
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