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In search of a mouse model for this disease, mutagenesis screens have identified several deletions that resemble these phenotypes. The\n                    <jats:italic>Hba<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>b2(th)<\/jats:italic>\n                    <\/jats:sup>\n                    deletion, in particular, replicates the characteristics of alpha-thalassemia minor in heterozygous mice but presents a homozygous embryonic lethal phenotype. Previous analyses of\n                    <jats:italic>Hba<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>b2(th)<\/jats:italic>\n                    <\/jats:sup>\n                    mice suggested that the deletion affects both\n                    <jats:italic>Hba<\/jats:italic>\n                    genes (\n                    <jats:italic>Hba-a1<\/jats:italic>\n                    and\n                    <jats:italic>Hba-a2<\/jats:italic>\n                    ) and considered epidermal growth factor receptor (\n                    <jats:italic>Egfr<\/jats:italic>\n                    ) or rhomboid 5 homolog 1 (\n                    <jats:italic>Rhbdf1<\/jats:italic>\n                    ) to be responsible for the embryonic lethality. Molecular analysis of\n                    <jats:italic>Hba<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>b2(th)<\/jats:italic>\n                    <\/jats:sup>\n                    revealed a deletion spanning a 1\u00a0cM region of mouse chromosome 11. Importantly, the\n                    <jats:italic>Hba<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>b2(th)<\/jats:italic>\n                    <\/jats:sup>\n                    deletion does not extend to\n                    <jats:italic>Egfr<\/jats:italic>\n                    , indicating that the observed lethality of homozygous embryos is not due to the loss of\n                    <jats:italic>Egfr<\/jats:italic>\n                    . Sequence analysis of the\n                    <jats:italic>Hba<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>b2(th)<\/jats:italic>\n                    <\/jats:sup>\n                    deletion showed that the\n                    <jats:italic>Hba-a2<\/jats:italic>\n                    gene is not deleted, but the lack of expression is likely due to the disruption of upstream regulatory regions. Furthermore, we identify\n                    <jats:italic>Snrnp2<\/jats:italic>\n                    5, which codes for the small nuclear ribonucleoprotein 25 (U11\/U12), as the candidate gene most likely responsible for the peri-implantation lethality of\n                    <jats:italic>Hba<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>b2(th)<\/jats:italic>\n                    <\/jats:sup>\n                    homozygous mice. These findings enhance the understanding of the genetic mechanisms underlying \u03b1-thalassemia and provide insights into novel genes essential for early mammalian development.\n                  <\/jats:p>","DOI":"10.1007\/s00335-025-10133-z","type":"journal-article","created":{"date-parts":[[2025,5,21]],"date-time":"2025-05-21T15:11:12Z","timestamp":1747840272000},"page":"727-734","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Snrnp25 is a candidate for the peri-implantation lethal phenotype of the Hba deletions"],"prefix":"10.1007","volume":"36","author":[{"given":"Ana Mar\u00eda","family":"Vel\u00e1squez-Escobar","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew E.","family":"Hillhouse","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Terry","family":"Magnuson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David W.","family":"Threadgill","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2025,5,21]]},"reference":[{"key":"10133_CR1","doi-asserted-by":"publisher","first-page":"1586","DOI":"10.1182\/blood.V80.6.1586.1586","volume":"80","author":"M Albitar","year":"1992","unstructured":"Albitar M, Care A, Peschle C, Liebhaber SA (1992) Developmental switching of messenger RNA expression from the human \u03b1-Globin cluster: fetal\/adult pattern of \u03b8-Globin gene expression. 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