Robustness mechanisms for gene expression though the paralogous genes

2014 Fiscal Year Final Research Report

• Project/Area Number: 24770214
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Developmental biology
• Research Institution: Yamagata University
• Principal Investigator: OCHI Haruki 山形大学, 医学部, 助教 (00505787)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: パラログ / 発生制御遺伝子 / Pax2 / Pax5 / ナメクジウオ / ツメガエル / トランスジェニックシステム / 浸透圧ストレス

Outline of Final Research Achievements

Paralogus genes often have redundant functions, while little is known about the evolution of their regulatory interactions. It has been reported that, while pax2 and ancestral-type ortholog pax2/5/8 show constitutive expression in the pronephros and its orthologous tissue in amphioxus respectively, pax5 shows no expression in the pronephros. We found that pax5 gets activated in the pronephros, by either the down-regulation of pax2, or by hypertonic osmotic stress. We identified a pronephric enhancer of pax2, and revealed that its paralogous counterpart in pax5 is involved in both the functional compensation of pax2 and the osmotic stress response. Their ancestral-type enhancer in pax2/5/8 was also active in the normal pronephros but got further activated by the hypertonic osmotic stress. These results suggest that the mechanisms for the functional compensation of pax2 by pax5 evolved from the osmotic stress response mechanism of their ancestral gene.

Free Research Field

遺伝子発現制御