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Biology subjects

Jäck, H.-M.

Publications and source records attributed to Jäck, H.-M..

4 recordsLinked to original sources

microRNAs control temporal patterning of the vertebrate nervous system

Temporal patterning is essential for generation of neuronal diversity in the developing vertebrate nervous system. A shared sequence of temporal transcription factors (tTFs) partitions neurons by birth date across much of the central nervous system. The molecular mechanisms that control the timing of expression of these tTFs are incompletely understood. Here, we provide evidence that this process is under the control of microRNAs (miRNAs). Perturbing miRNA biogenesis by conditional deletion of Dgcr8 from the developing mouse nervous system extends the window during which neurons with early identities are generated, but abolishes late identities in the spinal cord, hindbrain and midbrain, and holds progenitors in an early transcriptional state. We further identify miRNAs of the let-7 and miR-9 families, which target transcriptional regulators of early progenitor and neuronal identities, as candidates for mediating this effect. Throughout the nervous system, levels of these miRNAs rise during the neurogenic period in progenitors, while levels in neurons correlate with their birth-date. Moreover, the sensitivity of tTF-encoding transcripts to miR-9 inversely correlates with their expression sequence, suggesting a model in which miR-9 controls the chronology of neuronal cell fate transitions by targeting specifiers of early progenitor and neuronal temporal identity in a level-dependent manner. Consistently, perturbations of miR-9 expression dynamics by gain and loss-of-function approaches perturb temporal patterning. Together, our results demonstrate a critical, evolutionary conserved role for miRNAs in temporal patterning and suggest that a temporal miR-9 expression gradient controls the timing of tTF expression in large parts of the developing vertebrate nervous system.

developmental biology↗

Broadly neutralizing SARS-CoV-2 antibodies through epitope-based selection from convalescent patients

Emerging variants of concern (VOCs) are threatening to limit the effectiveness of SARS-CoV-2 monoclonal antibodies and vaccines currently used in clinical practice; broadly neutralizing antibodies and strategies for their identification are therefore urgently required. Here we demonstrate that broadly neutralizing antibodies can be isolated from peripheral blood mononuclear cells (PBMCs) of convalescent patients using SARS-CoV-2 receptor binding domains (RBDs) carrying epitope-specific mutations. This is exemplified by two human antibodies, GAR05, binding to epitope class 1, and GAR12, binding to a new epitope class 6 (located between class 3 and class 5). Both antibodies broadly neutralize VOCs, exceeding the potency of the clinical monoclonal sotrovimab (mAb S309) by orders of magnitude. They also provide potent prophylactic and therapeutic in vivo protection of hACE2 mice against viral challenge. Our results indicate that exposure to Wuhan SARS-CoV-2 induces antibodies that maintain potent and broad neutralization against emerging VOCs using two unique strategies: either by targeting the divergent class 1 epitope in a manner resistant to VOCs (ACE2 mimicry, as illustrated by GAR05 and mAbs P2C-1F11/S2K14); or alternatively, by targeting rare and highly conserved epitopes, such as the new class 6 epitope identified here (as illustrated by GAR12). Our results provide guidance for next generation monoclonal antibody development and vaccine design.

immunology↗

The microRNA processing subunit DGCR8 is required for a T cell-dependent germinal center response

We have previously shown that the microRNA (miRNA) processor complex consisting of the RNAse Drosha and the DiGeorge Critical Region (DGCR) 8 protein is essential for central B cell maturation. To determine whether miRNA processing is required to initiate T cell-mediated antibody responses, we deleted DGCR8 in maturing B-2 cells by crossing a mouse with loxP-flanked DGCR8 alleles with a CD23-Cre mouse. As expected, non-immunized mice showed reduced numbers of mature B-2 cells and IgG-secreting cells and diminished serum IgG titers. In accordance, germinal centers and antigen-specific IgG-secreting cells were absent in mice immunized with T cell-dependent antigens. Therefore, DGCR8 is required to mount an efficient T cell-dependent antibody response. However, DGCR8 deletion in B-1 cells was incomplete, which explains relatively unaffected B-1 cell numbers and adequate IgM and IgA titers in DGCR8-knock out mice and suggests that this mouse model could be used to analyze B-1 responses in the absence of functional B-2 cells.

immunology↗

The Omicron variant is highly resistant against antibody-mediated neutralization - implications for control of the COVID-19 pandemic

The rapid spread of the SARS-CoV-2 Omicron variant suggests that the virus might become globally dominant. Further, the high number of mutations in the viral spike-protein raised concerns that the virus might evade antibodies induced by infection or vaccination. Here, we report that the Omicron spike was resistant against most therapeutic antibodies but remained susceptible to inhibition by Sotrovimab. Similarly, the Omicron spike evaded neutralization by antibodies from convalescent or BNT162b2-vaccinated individuals with 10- to 44-fold higher efficiency than the spike of the Delta variant. Neutralization of the Omicron spike by antibodies induced upon heterologous ChAdOx1/BNT162b2-vaccination or vaccination with three doses of BNT162b2 was more efficient, but the Omicron spike still evaded neutralization more efficiently than the Delta spike. These findings indicate that most therapeutic antibodies will be ineffective against the Omicron variant and that double immunization with BNT162b2 might not adequately protect against severe disease induced by this variant.

microbiology↗