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3. Developmental loss of ErbB4 in PV interneurons disrupts state-dependent cortical circuit dynamics

Author

Batista-Brito, Renata, Majumdar, Antara, Nuno, Alejandro, Vinck, Martin, Cardin, Jessica A., Batista-Brito, Renata, Majumdar, Antara, Nuno, Alejandro, Vinck, Martin, and Cardin, Jessica A.

Abstract

GABAergic inhibition plays an important role in the establishment and maintenance of cortical circuits during development. Neuregulin 1 (Nrg1) and its interneuron-specific receptor ErbB4 are key elements of a signaling pathway critical for the maturation and proper synaptic connectivity of interneurons. Using conditional deletions of the ERBB4 gene in mice, we tested the role of this signaling pathway at two developmental timepoints in parvalbumin-expressing (PV) interneurons, the largest subpopulation of cortical GABAergic cells. Loss of ErbB4 in PV interneurons during embryonic, but not late postnatal, development leads to alterations in the activity of excitatory and inhibitory cortical neurons, along with severe disruption of cortical temporal organization. These impairments emerge by the end of the second postnatal week, prior to the complete maturation of the PV interneurons themselves. Early loss of ErbB4 in PV interneurons also results in profound dysregulation of excitatory pyramidal neuron dendritic architecture and a redistribution of spine density at the apical dendritic tuft. In association with these deficits, excitatory cortical neurons exhibit normal tuning for sensory inputs, but a loss of state-dependent modulation of the gain of sensory responses. Together these data support a key role for early developmental Nrg1/ErbB4 signaling in PV interneurons as powerful mechanism underlying the maturation of both the inhibitory and excitatory components of cortical circuits.

Published
2020

4. A conserved requirement forFbxo7during male germ cell cytoplasmic remodelling

Author

Rathje, Claudia Cattoni, Randle, Suzanne J, Al Rawi, Sara, Skinner, Benjamin Matthew, Nelson, David E, Majumdar, Antara, Johnson, Emma EP, Bacon, Joanne, Vlazaki, Myrto, Affara, Nabeel A, Ellis, Peter J.I., and Laman, Heike

Subjects
0303 health sciences, Cell type, biology, Spermatid, Spermiogenesis, Cell cycle, Chromatin, Ubiquitin ligase, Cell biology, 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Proteasome, biology.protein, medicine, 030217 neurology & neurosurgery, Germ cell, 030304 developmental biology
Abstract

Fbxo7 is the substrate-recognition subunit of an SCF-type ubiquitin E3 ligase complex. It has physiologically important functions in regulating mitophagy, proteasome activity and the cell cycle in multiple cell types, like neurons, lymphocytes and erythrocytes. Here, we show that in addition to the previously known Parkinsonian and hematopoietic phenotypes, male mice with reduced Fbxo7 expression are sterile. In these males, despite successful meiosis, nuclear elongation and eviction of histones from chromatin, the developing spermatids are phagocytosed by Sertoli cells during late spermiogenesis, as the spermatids undergo cytoplasmic remodeling. Surprisingly, despite the loss of all germ cells, there was no evidence of the symplast formation and cell sloughing that is typically associated with spermatid death in other mouse sterility models, suggesting that novel cell death and/or cell disposal mechanisms may be engaged in Fbxo7 mutant males. Mutation of the Drosophila Fbxo7 ortholog, nutcracker (ntc) also leads to sterility with germ cell death during cytoplasmic remodeling, indicating that the requirement for Fbxo7 at this stage is conserved. The ntc phenotype was attributed to decreased levels of the proteasome regulator, DmPI31 and reduced proteasome activity. Consistent with the fly model, we observe a reduction in PI31 levels in mutant mice; however, there is no alteration in proteasome activity in whole mouse testes. Our results are consistent with findings that Fbxo7 regulates PI31 protein levels, and indicates that a defect at the late stages of spermiogenesis, possibly due to faulty spatial dynamics of proteasomes during cytoplasmic remodeling, may underlie the fertility phenotype in mice.

Published
2019
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5. A Conserved Requirement for Fbxo7 During Male Germ Cell Cytoplasmic Remodeling

Author

Rathje, Claudia C., primary, Randle, Suzanne J., additional, Al Rawi, Sara, additional, Skinner, Benjamin M., additional, Nelson, David E., additional, Majumdar, Antara, additional, Johnson, Emma E. P., additional, Bacon, Joanne, additional, Vlazaki, Myrto, additional, Affara, Nabeel A., additional, Ellis, Peter J., additional, and Laman, Heike, additional

Published
2019
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6. Viable mouse gene ablations that robustly alter brain Aβ levels are rare

Author

Small Daniel L, Majumdar Antara, Corradi John, Barrezueta Nestor, Sankaranarayanan Sethu, Meredith Jere E, Guss Valerie, Thompson Mark W, Lin Xu-Alan, Toyn Jeremy H, Hansard Melissa, Lanthorn Thomas, Westphal Ryan S, and Albright Charles F

Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571, Neurophysiology and neuropsychology, QP351-495
Abstract

Abstract Background Accumulation of amyloid-β (Aβ) peptide in the brain is thought to play a key pathological role in Alzheimer's disease. Many pharmacological targets have therefore been proposed based upon the biochemistry of Aβ, but not all are equally tractable for drug discovery. Results To search for novel targets that affect brain Aβ without causing toxicity, we screened mouse brain samples from 1930 novel gene knock-out (KO) strains, representing 1926 genes, using Aβ ELISA assays. Although robust Aβ lowering was readily apparent in brains from a BACE1 KO strain, none of the novel strains exhibited robust decreases in brain Aβ, including a GPR3 KO strain, which had previously been proposed as an Aβ target. However, significantly increased Aβ was observed in brain samples from two KO strains, corresponding to genes encoding the glycosylphosphatidylinositol mannosyl transferase PIGZ and quinolinate phosphoribosyltransferase (QPRT). Conclusions Thus, gene ablations that are permissive for mouse survival and that also have a robust effect on Aβ levels in the brain are rare.

Published
2010
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7. In Vitro Antiviral Characteristics of HIV-1 Attachment Inhibitor BMS-626529, the Active Component of the Prodrug BMS-663068

Author

Nowicka-Sans, Beata, primary, Gong, Yi-Fei, additional, McAuliffe, Brian, additional, Dicker, Ira, additional, Ho, Hsu-Tso, additional, Zhou, Nannan, additional, Eggers, Betsy, additional, Lin, Pin-Fang, additional, Ray, Neelanjana, additional, Wind-Rotolo, Megan, additional, Zhu, Li, additional, Majumdar, Antara, additional, Stock, David, additional, Lataillade, Max, additional, Hanna, George J., additional, Matiskella, John D., additional, Ueda, Yasutsugu, additional, Wang, Tao, additional, Kadow, John F., additional, Meanwell, Nicholas A., additional, and Krystal, Mark, additional

Published
2012
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8. Viable mouse gene ablations that robustly alter brain Aβ levels are rare

Author

Toyn, Jeremy H, primary, Lin, Xu-Alan, additional, Thompson, Mark W, additional, Guss, Valerie, additional, Meredith, Jere E, additional, Sankaranarayanan, Sethu, additional, Barrezueta, Nestor, additional, Corradi, John, additional, Majumdar, Antara, additional, Small, Daniel L, additional, Hansard, Melissa, additional, Lanthorn, Thomas, additional, Westphal, Ryan S, additional, and Albright, Charles F, additional

Published
2010
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9. In VitroAntiviral Characteristics of HIV-1 Attachment Inhibitor BMS-626529, the Active Component of the Prodrug BMS-663068

Author

Nowicka-Sans, Beata, Gong, Yi-Fei, McAuliffe, Brian, Dicker, Ira, Ho, Hsu-Tso, Zhou, Nannan, Eggers, Betsy, Lin, Pin-Fang, Ray, Neelanjana, Wind-Rotolo, Megan, Zhu, Li, Majumdar, Antara, Stock, David, Lataillade, Max, Hanna, George J., Matiskella, John D., Ueda, Yasutsugu, Wang, Tao, Kadow, John F., Meanwell, Nicholas A., and Krystal, Mark

Abstract

ABSTRACTBMS-663068 is the phosphonooxymethyl prodrug of BMS-626529, a novel small-molecule attachment inhibitor that targets HIV-1 gp120 and prevents its binding to CD4+T cells. The activity of BMS-626529 is virus dependent, due to heterogeneity within gp120. In order to better understand the anti-HIV-1 spectrum of BMS-626529 against HIV-1, in vitroactivities against a wide variety of laboratory strains and clinical isolates were determined. BMS-626529 had half-maximal effective concentration (EC50) values of <10 nM against the vast majority of viral isolates; however, susceptibility varied by >6 log10, with half-maximal effective concentration values in the low pM range against the most susceptible viruses. The in vitroantiviral activity of BMS-626529 was generally not associated with either tropism or subtype, with few exceptions. Measurement of the binding affinity of BMS-626529 for purified gp120 suggests that a contributory factor to its inhibitory potency may be a relatively long dissociative half-life. Finally, in two-drug combination studies, BMS-626529 demonstrated additive or synergistic interactions with antiretroviral drugs of different mechanistic classes. These results suggest that BMS-626529 should be active against the majority of HIV-1 viruses and support the continued clinical development of the compound.

Published
2012
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