Gene redundancy and gene compensation: an updated view

Publication date: Available online 19 July 2019Source: Journal of Genetics and GenomicsAuthor(s): Jinrong PengAbstractGene 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-of-function or gain-of-function mutants. The fast development of gene 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 organism including 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 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.

Source: Journal of Genetics and Genomics - July 20, 2019 Category: Genetics & Stem Cells Source Type: research