Figure 2.

Development of the Brattleboro rat strain. (A) Brattleboro rat strain was discovered in 1961 in Brattleboro, Vermont. It evolved from the Long–Evans rat strain through a random autosomal recessive mutation. (B) The genetic mutation of Brattleboro strain is a single nucleotide deletion of a G residue in the second exon of neurophysin gene. Due to this mutation, a reading frame shift develops, which results in different C-terminus for the precursor hormone. (C) Due to the lack of stop codon, the mRNA cannot leave the ribosomes after translation, and the incomplete protein-chain might also stall in the ribosome. Therefore, a ubiquitin ligase (LTN1), which is part of the ribosome-associated quality control complex, will induce proteolysis. All in all, vasopressin (AVP) is missing; thus, there is no physiologically active central AVP, leading to central diabetes insipidus with polydipsia and polyuria [41,42,43,44,45].