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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,6,9]]},"abstract":"<jats:p>\n                    Chondrodysplasia is a genetic disorder characterized by impaired cartilage development and bone growth. Dysregulation of the endoplasmic reticulum (ER) stress is associated with chondrodysplasia. Here, we demonstrate a critical role for the ER stress regulator PPP1R15B in chondrocyte development. PPP1R15B is a protein phosphatase that constitutively represses eIF2\u03b1 phosphorylation to attenuate global protein translation in response to stress. Remarkably, deletion of\n                    <jats:italic toggle=\"yes\">Ppp1r15b<\/jats:italic>\n                    in\n                    <jats:italic toggle=\"yes\">\n                      Prx1\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:italic>\n                    skeletal progenitors (\n                    <jats:italic toggle=\"yes\">\n                      Ppp1r15b\n                      <jats:sup>Prx1<\/jats:sup>\n                    <\/jats:italic>\n                    ) impairs chondrogenesis, resulting in a disorganized growth plate, reduced trabecular bone, and shortened long bones in mice. Similarly, inducible deletion of\n                    <jats:italic toggle=\"yes\">Ppp1r15b<\/jats:italic>\n                    in\n                    <jats:italic toggle=\"yes\">\n                      Col2\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:italic>\n                    chondroprogenitors (\n                    <jats:italic toggle=\"yes\">\n                      Ppp1r15b\n                      <jats:sup>Col2<\/jats:sup>\n                    <\/jats:italic>\n                    ) leads to abnormal cartilage development and bone growth. Remarkably, no skeletal phenotype is observed in mice lacking\n                    <jats:italic toggle=\"yes\">Ppp1r15b<\/jats:italic>\n                    in committed\n                    <jats:italic toggle=\"yes\">\n                      Osx\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:italic>\n                    osteoprogenitors (\n                    <jats:italic toggle=\"yes\">\n                      Ppp1r15b\n                      <jats:sup>Osx<\/jats:sup>\n                    <\/jats:italic>\n                    ) and\n                    <jats:italic toggle=\"yes\">\n                      Dmp1\n                      <jats:sup>+<\/jats:sup>\n                    <\/jats:italic>\n                    mature osteoblasts and osteocytes (\n                    <jats:italic toggle=\"yes\">\n                      Ppp1r15b\n                      <jats:sup>Dmp1<\/jats:sup>\n                    <\/jats:italic>\n                    ), indicating that its role is limited to regulation of chondrogenesis, not osteogenic differentiation. Mechanistically, PPP1R15B deletion increases eIF2\u03b1 phosphorylation, which in turn enhances lipogenic gene expression by suppressing leptin expression. This effect was reversed in\n                    <jats:italic toggle=\"yes\">\n                      Ppp1r15b\n                      <jats:sup>Prx1<\/jats:sup>\n                    <\/jats:italic>\n                    mice by reconstitution with wild-type PPP1R15B, but not with a mutant form incapable of eIF2\u03b1 dephosphorylation. Exogenous expression of leptin also reversed skeletal abnormalities in these mice. Collectively, these findings reveal a critical role for PPP1R15B in cartilage development through its regulation of lipid metabolism.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2600080123","type":"journal-article","created":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T19:33:41Z","timestamp":1780342421000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Control of lipid metabolism in chondrocytes is critical for skeletal growth"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8261-2742","authenticated-orcid":false,"given":"Aijaz Ahmad","family":"John","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0464eyp60","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Genetic and Cellular Medicine, University of Massachusetts Chan Medical 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