Pradeep M Joshi

University of California, Santa Barbara, Santa Barbara, CA, United States

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Publications (3)21.58 Total impact

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    ABSTRACT: We review the application of Caenorhabditis elegans as a model system to understand key aspects of stem cell biology. The only bona fide stem cells in C. elegans are those of the germline, which serves as a valuable paradigm for understanding how stem-cell niches influence maintenance and differentiation of stem cells and how somatic differentiation is repressed during germline development. Somatic cells that share stem cell–like characteristics also provide insights into principles in stem-cell biology. The epidermal seam cell lineages lend clues to conserved mechanisms of self-renewal and expansion divisions. Principles of developmental plasticity and reprogramming relevant to stem-cell biology arise from studies of natural transdifferentiation and from analysis of early embryonic progenitors, which undergo a dramatic transition from a pluripotent, reprogrammable condition to a state of committed differentiation. The relevance of these developmental processes to our understanding of stem-cell biology in other organisms is discussed. Developmental Dynamics 239:1539–1554, 2010. © 2010 Wiley-Liss, Inc.
    Developmental Dynamics 04/2010; 239(5):1539 - 1554. · 2.59 Impact Factor
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    ABSTRACT: Cell-size-control systems, coupled with apoptotic- and cell-proliferation-regulatory mechanisms, determine the overall dimensions of organs and organisms, and their dysregulation can lead to tumor formation. The interrelationship between cell-growth-regulatory mechanisms and apoptosis during normal development and cancer is not understood. The TRK-fused gene (TFG) promotes tumorigenesis when present in chromosomal rearrangements from various human-cancer types by unknown mechanisms. Apaf1/CED-4 is essential for apoptosis but has not been shown to function in cell-growth control. We found that loss of TFG-1, the TFG ortholog in Caenorhabditis elegans, results in supernumerary apoptotic corpses, whereas its overexpression is sufficient to inhibit developmentally programmed cell death. TFG-1 is also required for cells and nuclei to grow to normal size. Furthermore, we found that CED-4 is required for cell-growth inhibition in animals lacking TFG-1. However, caspases, the downstream effectors of CED-4-mediated apoptosis, are not required in TFG-1- or CED-4-regulated cell-size control. CED-4 acts to inhibit cell growth by antagonizing the effects of other conserved cell-size-regulating proteins, including cAMP response element binding (CREB) protein, translation-initiation factor eIF2B, and the nucleolar p53-interacting protein nucleostemin. These findings show that TFG-1 suppresses apoptosis and is essential for normal cell-size control, suggesting that abnormalities in the cell-growth-promoting and apoptosis-inhibiting functions of TFG might be responsible for its action in tumorigenesis. Also, they reveal that CED-4 plays a pivotal role in activating apoptosis and restricting cell and nuclear size, thereby determining the appropriate overall size of an animal. Thus, these findings reveal links between the control mechanisms for apoptosis and cell growth.
    Current Biology 07/2008; 18(14):1025-33. · 9.49 Impact Factor
  • Pradeep M Joshi, Joel H Rothman
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    ABSTRACT: During gastrulation of the nematode worm Caenorhabditis elegans, individual cells ingress into a solid ball of cells. Gastrulation in a basal nematode, in contrast, has now been found to occur by invagination into a blastocoel, revealing an unanticipated embryological affinity between nematodes and all other triploblastic metazoans.
    Current Biology 08/2005; 15(13):R495-8. · 9.49 Impact Factor

Publication Stats

30 Citations
21.58 Total Impact Points

Institutions

  • 2005–2010
    • University of California, Santa Barbara
      • • Neuroscience Research Institute
      • • Department of Molecular, Cellular, and Developmental Biology
      Santa Barbara, CA, United States
  • 2008
    • Molecular and Cellular Biology Program
      Seattle, Washington, United States