• Prim B Singh

      Articles written in Journal of Biosciences

    • A hypomorphic Cbx3 allele causes prenatal growth restriction and perinatal energy homeostasis defects

      Ebru Aydin Dick-Paul Kloos Emmanuel Gay Willem Jonker Lijuan Hu Jörn Bullwinkel Jeremy P Brown Maria Manukyan Martin Giera Prim B Singh Reinald Fundele

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      Mammals have three HP1 protein isotypes HP1𝛽 (CBX1), HP1𝛾 (CBX3) and HP1𝛼 (CBX5) that are encoded by the corresponding genes Cbx1, Cbx3 and Cbx5. Recent work has shown that reduction of CBX3 protein in homozygotes for a hypomorphic allele (Cbx3hypo) causes a severe postnatal mortality with around 99% of the homozygotes dying before weaning. It is not known what the causes of the postnatal mortality are. Here we show that Cbx3hypo/hypo conceptuses are significantly reduced in size and the placentas exhibit a haplo-insufficiency. Late gestation Cbx3hypo/hypo placentas have reduced mRNA transcripts for genes involved in growth regulation, amino acid and glucose transport. Blood vessels within the Cbx3hypo/hypo placental labyrinth are narrower than wild-type. Newborn Cbx3hypo/hypo pups are hypoglycemic, the livers are depleted of glycogen reserves and there is almost complete loss of stored lipid in brown adipose tissue (BAT). There is a 10-fold reduction in expression of the BAT-specific Ucp1 gene, whose product is responsible for non-shivering themogenesis. We suggest that it is the small size of the Cbx3hypo/hypo neonates, a likely consequence of placental growth and transport defects, combined with a possible inability to thermoregulate that causes the severe postnatal mortality.

    • Heterochromatin and the molecular mechanisms of ‘parent-of-origin’ effects in animals


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      Twenty five years ago it was proposed that conserved components of constitutive heterochromatin assemble heterochromatinlikecomplexes in euchromatin and this could provide a general mechanism for regulating heritable (cell-to-cell) changesin gene expressibility. As a special case, differences in the assembly of heterochromatin-like complexes on homologouschromosomes might also regulate the parent-of-origin-dependent gene expression observed in placental mammals. Here,the progress made in the intervening period with emphasis on the role of heterochromatin and heterochromatin-likecomplexes in parent-of-origin effects in animals is reviewed.

    • Deconstructing age reprogramming


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      It has been proposed that age reprogramming enables old cells to be rejuvenated without passage through an embryonicstage (Singh and Zacouto in J. Biosci. 35 315–319, 2010). As such, age reprogramming stands apart from the inducedpluripotent stem (iPS) and nuclear transfer-embryonic stem (NT-ES) cell therapies where histo-compatible cells are producedonly after passage through an embryonic stage. It avoids many of the disadvantages associated with iPS and NT-EScell therapies. Experimental evidence in support of age reprogramming is burgeoning. Here, we discuss possible newapproaches to enhance age reprogramming, which will have considerable benefits for regenerative therapies.

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