Browsing by Author "Banik, Debarghya Dutta"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    EGR4 is critical for cell-fate determination and phenotypic maintenance of geniculate ganglion neurons underlying sweet and umami taste
    (National Academy of Science, 2023) Banik, Debarghya Dutta; Martin, Louis J.; Tang, Tao; Soboloff, Jonathan; Tourtellotte, Warren G.; Pierchala, Brian A.; Anatomy, Cell Biology and Physiology, School of Medicine
    The sense of taste starts with activation of receptor cells in taste buds by chemical stimuli which then communicate this signal via innervating oral sensory neurons to the CNS. The cell bodies of oral sensory neurons reside in the geniculate ganglion (GG) and nodose/petrosal/jugular ganglion. The geniculate ganglion contains two main neuronal populations: BRN3A+ somatosensory neurons that innervate the pinna and PHOX2B+ sensory neurons that innervate the oral cavity. While much is known about the different taste bud cell subtypes, considerably less is known about the molecular identities of PHOX2B+ sensory subpopulations. In the GG, as many as 12 different subpopulations have been predicted from electrophysiological studies, while transcriptional identities exist for only 3 to 6. Importantly, the cell fate pathways that diversify PHOX2B+ oral sensory neurons into these subpopulations are unknown. The transcription factor EGR4 was identified as being highly expressed in GG neurons. EGR4 deletion causes GG oral sensory neurons to lose their expression of PHOX2B and other oral sensory genes and up-regulate BRN3A. This is followed by a loss of chemosensory innervation of taste buds, a loss of type II taste cells responsive to bitter, sweet, and umami stimuli, and a concomitant increase in type I glial-like taste bud cells. These deficits culminate in a loss of nerve responses to sweet and umami taste qualities. Taken together, we identify a critical role of EGR4 in cell fate specification and maintenance of subpopulations of GG neurons, which in turn maintain the appropriate sweet and umami taste receptor cells.
  • Thumbnail Image
    Item
    Identification of a postnatal period of interdependent neurogenesis and apoptosis in peripheral neurons
    (The Company of Biologists, 2024) Kaminski, Catherine L.; Banik, Debarghya Dutta; Schmitd, Ligia B.; Pierchala, Brian A.; Anatomy, Cell Biology and Physiology, School of Medicine
    During neurogenesis, excessive numbers of neurons are produced in most regions of the central and peripheral nervous systems. Nonessential neurons are eliminated by apoptosis, or programmed cell death. This has been most thoroughly characterized in the peripheral nervous system (PNS) where targets of innervation play a key role in this process. As maturing neurons project axons towards their targets of innervation, they become dependent upon these targets for survival. Survival factors, also called neurotrophic factors, are produced by targets, inhibit apoptosis cascades, and promote further growth and differentiation. Because neurotrophic factors are limited, as is target size, neurons that do not correctly and efficiently innervate targets undergo apoptosis ( Levi-Montalcini, 1987; Davies, 1996). Thus, excessive neurogenesis acts to ensure that sufficient numbers of neurons are produced during development. In the superior cervical ganglion (SCG), this process of neurogenesis and subsequent apoptosis is reported to be complete by postnatal day 3-4 (P3-P4) in mice. Surprisingly, we observed significant numbers of apoptotic neurons out to P14, and neurogenesis was still present at P14 as well. In both the SCG and geniculate ganglion (GG), postnatal neurogenesis was dependent on apoptosis because little or no postnatal neurogenesis was observed in Bax-/- mice, in which apoptosis is eliminated. These results indicate that both neurogenesis and apoptosis continue to occur well after birth in peripheral ganglia, and that neurogenesis depends on apoptosis, suggesting that neurogenesis continues postnatally to replace neurons that are eliminated during synaptic refinement.