群馬大学生体調節研究所Research – 群馬大学生体調節研究所

【Press release】Identification of BCAS-3 as an important factor for paternal mitochondrial degradation

sysad — Mon, 15 Jun 2026 02:50:47 +0000

In this study, we show that BCAS3 is required for paternal mitochondrial degradation. BCAS3 is also conserved in humans, and mutations in this gene have been reported to cause neurodevelopmental disorder. Our findings not only reveal the mechanism of paternal mitochondrial degradation but may also contribute to understanding the pathogenesis of neurodevelopmental disorders caused by BCAS3 mutations.

For details of the research, please click here.

Identification of BCAS-3 as an important factor for paternal mitochondrial degradation

sysad — Mon, 15 Jun 2026 02:49:31 +0000

Mitochondria possess their own DNA, and mitochondrial DNA is maternally inherited in most organisms. We previously showed that autophagic degradation of paternal mitochondria is responsible for this unique inheritance in the nematode Caenorhabditis elegans. However, the molecular mechanism underlying this process has remained unclear.
In this study, we show that BCAS3 is required for paternal mitochondrial degradation. We also found that loss of BCAS3 function impaired accumulation of machinery required for autophagosome formation around paternal mitochondria, suggesting that BCAS3 plays an important role in autophagosome formation. BCAS3 is also conserved in humans, and mutations in this gene have been reported to cause neurodevelopmental disorders. Our findings not only reveal the mechanism of paternal mitochondrial degradation but may also contribute to understanding the pathogenesis of neurodevelopmental disorders caused by BCAS3 mutations.

開催報告[内分泌・代謝学共同利用共同研究拠点セミナー] 順天堂大学名誉教授河盛隆造先生ご講演

sysad — Fri, 15 May 2026 04:50:32 +0000

2026年5月15日、順天堂大学名誉教授河盛　隆造先生をお招きし、「一瞬、一瞬がドラマ、楽しかった私の大学生活６０年！」というタイトルでご講演いただきました。

【Press release】Amino Acid Metabolism Regulates Hormone Secretion in the Body

sysad — Tue, 12 May 2026 04:21:10 +0000

A research group led by Professor Takashi Nishimura of the Laboratory of Metabolic Regulation and Genetics has elucidated part of the mechanism by which the secretion of a glucagon-like hormone is regulated by amino acid metabolism in the body, using the model organism Drosophila melanogaster.
This research is expected to provide important insights into how organisms coordinate energy metabolism and oxidative stress defense in response to nutritional conditions. In addition, findings obtained in insects may help advance our understanding of the mechanisms regulating glucagon secretion and amino acid metabolism disorders in mammals.

For details of the research, please click here.

Amino Acid Metabolism Regulates Hormone Secretion in the Body

sysad — Tue, 12 May 2026 04:19:54 +0000

Animals survive by storing nutrients from food and using them when needed. When food is scarce, such as during starvation, they break down stored fats and sugars to produce energy. In mammals, endocrine hormones such as insulin and glucagon play key roles in controlling these responses to changes in nutrition. In insects, a hormone called Akh has a function similar to that of glucagon.

In this study, the research team developed a highly sensitive method to measure Akh in Drosophila melanogaster and examined how Akh secretion is regulated during starvation. They found that Akh acts on an organ called the fat body, where it promotes the breakdown of branched-chain amino acids (BCAAs). They also showed that BCAA metabolism works as a feedback mechanism that prevents excessive Akh secretion. In addition, Akh-promoted BCAA metabolism was found to support not only amino acid breakdown, but also the synthesis of glutathione, an antioxidant, and protection against oxidative stress during starvation. These findings reveal a new mechanism by which hormone secretion, amino acid metabolism, and oxidative stress defense work together to help animals adapt to nutrient deficiency.

【Press release】Part of the Mechanism Behind Oocyte Formation Unveiled ~ Discovery of the ROOM Protein, Essential for Oocyte Compartment Formation ~

sysad — Fri, 08 May 2026 01:39:02 +0000

A research group led by Kenta Sugiura, Ichiro Kawasaki, and Professor Ken Sato (IMCR, Gunma University), in collaboration with Professor Hidetaka Kosako (Tokushima University), has shed light on a key mechanism underlying the formation of oocytes. This research is expected to bring us closer to unraveling the mysteries of cellular structure formation, which underpin the very foundations of life.

・Proceedings of National Academy of Sciences of United States of America 誌（PNAS社：米国）
・2026/5/5
・Transmembrane ROOM proteins ensure rooms for germ cells by maintaining intercellular bridge

For details of the research, please click here.

Part of the Mechanism Behind Oocyte Formation Unveiled ~ Discovery of the ROOM Protein, Essential for Oocyte Compartment Formation ~

sysad — Thu, 07 May 2026 06:42:26 +0000

The formation of oocytes (eggs) is an essential step in many animals. As oocytes mature, they undergo repeated incomplete cell division from a single cell, resulting in a state where multiple cells share components (known as a syncytium). While it is known in many organisms that actomyosin and proteins playing auxiliary roles are involved in the formation and maintenance of syncytium, many aspects of this process remained unclear. We have now discovered that when the ROOM-1 and ROOM-2 proteins are lacked in the nematode Caenorhabditis elegans, oocytes fail to form entirely, and the organism becomes unable to produce offspring. Detailed observations revealed that oocyte formation does not proceed because cellular compartments fail to form properly during the process of syngamy (Figure). Since ROOM proteins have a structure that anchors directly to the cell membrane, this suggests that ROOM proteins anchor to the boundary of the oocyte to fix actomyosin, thereby maintaining incomplete cell division.

【Press release】Metformin suppresses β-cell apoptosis under ER stress by inhibiting protein translation

sysad — Fri, 10 Apr 2026 04:21:38 +0000

Endoplasmic reticulum (ER) stress is a critical driver of pancreatic β-cell dysfunction and apoptosis. Although metformin, a drug used to treat type 2 diabetes, primarily decreases blood glucose levels by improving insulin sensitivity, its direct effects on β-cell survival remain unclear. Here, we investigated the effect of metformin on β-cell stress responses under ER stress conditions. Thapsigargin (Tg)-induced ER stress increased β-cell apoptosis in mouse islets, which was prevented by metformin in a dose-dependent manner. Treatment with metformin for 24 h suppressed the Tg-induced upregulation of unfolded protein response (UPR)-related genes, as confirmed by transcriptomic and pathway analyses. Quantitative proteomics revealed that Tg inhibited eIF2 signaling and protein translation, both of which were partially restored by metformin. Enrichment analysis further indicated the attenuation of apoptotic pathways in metformin-treated islets. Polysome profiling and puromycin incorporation assays demonstrated that metformin reduced protein translation independently of ER stress. Metformin promoted the dephosphorylation of 4E-BP1, a key initiator of cap-dependent protein translation that is activated by phosphorylation, and the antiapoptotic effect of metformin was abolished by 4E-BP1 knockdown in MIN6 cells. Taken together, these findings reveal a cytoprotective mechanism of metformin in β-cells, in which metformin suppresses ER stress-induced apoptosis through 4E-BP1-mediated inhibition of mRNA translation. This study highlights a β-cell-intrinsic action of metformin that may contribute to its long-term therapeutic benefits in diabetes management.

・Metabolism
・2026/4/8
・Metformin suppresses β-cell apoptosis under ER stress by inhibiting protein translation

For details of the research, please click here.

Metformin suppresses β-cell apoptosis under ER stress by inhibiting protein translation

sysad — Fri, 10 Apr 2026 04:20:02 +0000

[20260514]Joint/Usage Research Program Seminar

sysad — Mon, 06 Apr 2026 06:15:28 +0000

” 一瞬、一瞬がドラマ、楽しかった私の大学生活６０年！”

Ryuzo Kawamori, M.D., Ph.D.
Juntendo University

Thursday, May 14 ^th, 2026 16:00~
IMCR Gunma Univ. 1F Conference Room

Click here

群馬大学 生体調節研究所Research – 群馬大学 生体調節研究所

【Press release】Identification of BCAS-3 as an important factor for paternal mitochondrial degradation

Identification of BCAS-3 as an important factor for paternal mitochondrial degradation

開催報告[内分泌・代謝学共同利用共同研究拠点セミナー] 順天堂大学名誉教授 河盛 隆造 先生ご講演

【Press release】Amino Acid Metabolism Regulates Hormone Secretion in the Body

Amino Acid Metabolism Regulates Hormone Secretion in the Body

【Press release】Part of the Mechanism Behind Oocyte Formation Unveiled ~ Discovery of the ROOM Protein, Essential for Oocyte Compartment Formation ~

Part of the Mechanism Behind Oocyte Formation Unveiled ~ Discovery of the ROOM Protein, Essential for Oocyte Compartment Formation ~

【Press release】Metformin suppresses β-cell apoptosis under ER stress by inhibiting protein translation

Metformin suppresses β-cell apoptosis under ER stress by inhibiting protein translation

[20260514]Joint/Usage Research Program Seminar

群馬大学生体調節研究所Research – 群馬大学生体調節研究所

開催報告[内分泌・代謝学共同利用共同研究拠点セミナー] 順天堂大学名誉教授河盛隆造先生ご講演