2022 Fiscal Year Final Research Report
Exploration of genetic mechanisms for renal origin using failure of ureteral bud invasion mouse
| Project/Area Number |
19K09732
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Review Section |
Basic Section 56030:Urology-related
|
|---|
| Research Institution | University of Miyazaki |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
向井 尚一郎 宮崎大学, 医学部, 准教授 (10315369)
藤井 将人 宮崎大学, 医学部, 助教 (10794373)
寺田 直樹 宮崎大学, 医学部, 准教授 (60636637)
永井 崇敬 宮崎大学, 医学部, 助教 (60739994)
西野 光一郎 宮崎大学, 農学部, 教授 (90508144)
|
|---|
| Project Period (FY) |
2019-04-01 – 2023-03-31
|
| Keywords | 腎発生 / 腎形成不全 |
|---|
| Outline of Final Research Achievements |
We have collected genomic DNA from four groups. Whole-genome sequencing was performed using next-generation sequencers, and mutation and indel comparative analysis was conducted. As a result, we have identified 35 genomic regions as potential candidate regions for the cause of FUBI. Successful establishment of embryonic stem (ES) cells has been achieved from fertilized eggs of ddy and FUBI. Gene expression comparative analysis using microarray technology was performed on ddyES and FUBIES, revealing a difference in the number of probes, with 432 probes showing differences, and 37 of them located on chromosome 2.
Considering the observed frequency of alterations in the expression system of FUBI through FUBI breeding and in the mutation of Gn14325 across all FUBI groups (with both kidneys, one kidney, and no kidneys), it is possible that the appearance of the FUBI expression system is regulated by a mechanism similar to haploinsufficiency.
|
| Free Research Field |
泌尿器科学
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究を通して、FUBIマウスにおける腎形成不全の原因解析を行うことで、ヒトにおける腎尿路発生のメカニズムに迫ることができると考える。最終的には、発生頻度の比較的高い疾患である腎盂尿管移行部狭窄症をはじめとする先天性尿路奇形の原因の一部が解明され、それらの発生に関わる遺伝子群を同定することが出来れば、その早期診断が可能となる。
|
