Elisa Thoral, Maria Gomez Correia, Imen Chamkha, Eskil Elmér, Andreas Nord
{"title":"Incubation temperature shapes growth and mitochondrial metabolism across embryonic development in Japanese quail.","authors":"Elisa Thoral, Maria Gomez Correia, Imen Chamkha, Eskil Elmér, Andreas Nord","doi":"10.1098/rspb.2025.1752","DOIUrl":null,"url":null,"abstract":"<p><p>Incubation temperature affects both growth and energy metabolism in birds after hatching. Changes in cellular mechanisms, including mitochondrial function, are a likely but unexplored explanation for these effects. To test whether temperature-dependent changes to mitochondria may link embryonic development to the post-natal phenotype, we incubated Japanese quail eggs at constant low (36.0°C), medium (37.5°C) or high (39.0°C) temperature and studied mitochondrial function and growth during embryogenesis and at hatching. Embryos grew faster and had higher mitochondrial metabolism at the high incubation temperature. Low incubation temperature slowed embryonic development and decreased phosphorylating respiration but was associated with higher adenosine triphosphate production efficiency. These respiration changes were mirrored by differences in mitochondrial content, which was the lowest in cold embryos. Neither treatment affected reactive oxygen species production. Hence, improved coupling efficiency in cold embryos may have partially compensated for lower adenosine triphosphate production without increasing oxidative stress. Size differences had disappeared by hatching. However, cold-incubated chicks had a higher mitochondrial content compared with the other groups. Our study suggests that thermal suppression of embryonic metabolism may be compensated by a combination of increased coupling, longer developmental time and late-occurring upregulation of mitochondrial content. The long-term implications of these results should be studied further.</p>","PeriodicalId":520757,"journal":{"name":"Proceedings. Biological sciences","volume":"292 2054","pages":"20251752"},"PeriodicalIF":3.5000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12419889/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proceedings. Biological sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1098/rspb.2025.1752","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/9/10 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Incubation temperature affects both growth and energy metabolism in birds after hatching. Changes in cellular mechanisms, including mitochondrial function, are a likely but unexplored explanation for these effects. To test whether temperature-dependent changes to mitochondria may link embryonic development to the post-natal phenotype, we incubated Japanese quail eggs at constant low (36.0°C), medium (37.5°C) or high (39.0°C) temperature and studied mitochondrial function and growth during embryogenesis and at hatching. Embryos grew faster and had higher mitochondrial metabolism at the high incubation temperature. Low incubation temperature slowed embryonic development and decreased phosphorylating respiration but was associated with higher adenosine triphosphate production efficiency. These respiration changes were mirrored by differences in mitochondrial content, which was the lowest in cold embryos. Neither treatment affected reactive oxygen species production. Hence, improved coupling efficiency in cold embryos may have partially compensated for lower adenosine triphosphate production without increasing oxidative stress. Size differences had disappeared by hatching. However, cold-incubated chicks had a higher mitochondrial content compared with the other groups. Our study suggests that thermal suppression of embryonic metabolism may be compensated by a combination of increased coupling, longer developmental time and late-occurring upregulation of mitochondrial content. The long-term implications of these results should be studied further.