Apoptosis and development by Hermann Steller

By Hermann Steller

Apoptosis and Development, the newest quantity of Current themes in Developmental Biology maintains the legacy of this most well known serial with caliber chapters authored by way of leaders within the box.

This quantity covers examine tools in apoptosis and improvement, and comprises sections on such subject matters because the non-lethal function of apoptotic proteins and germ line cellphone loss of life in Drosophila.

  • Continues the legacy of this most advantageous serial with caliber chapters authored by means of leaders within the field
  • Includes descriptions of the newest advances within the field
  • Covers learn tools in apoptosis and improvement, and comprises sections on such themes because the non-lethal position of apoptotic proteins and germ line phone demise in Drosophila

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Direct regulation of egl-1 and of programmed cell death by the Hox protein MAB-5 and by CEH-20, a C. elegans homolog of Pbx1. Development, 133, 641–650. Lockshin, R. , & Williams, C. M. (1965). Programmed cell death—I. Cytology of degeneration in the intersegmental muscles of the pernyi silkmoth. Journal of Insect Physiology, 11, 123–133. , Rolland, S. , & Conradt, B. (2011). A molecular switch that governs mitochondrial fusion and fission mediated by the BCL2-like protein CED-9 of Caenorhabditis elegans.

Death may allow fusion of the gonad with the cloaca, resulting in an open germ system competent for sperm transfer during fertilization. , 1983); however, later studies demonstrated that the cell can die following ablation of these dedicated engulfing cells, or in animals in which the linker cell fails to migrate properly (Abraham, Lu, & Shaham, 2007). Anecdotal reports also suggested initially that linker cell death is partially dependent on ced-3 and ced-4 (Ellis & Horvitz, 1986). However, further studies of the genetic requirements for death, coupled with extensive morphological and ultrastructural observations, revealed that linker cell death does not require ced-3 or ced-4.

Elegans. Journal of Cell Science, 123, 2001–2007. Osterloh, J. , Rooney, T. , Fox, A. , Powell, E. , et al. (2012). dSarm/Sarm1 is required for activation of an injury-induced axon death pathway. Science, 337, 481–484. , & Chamberlin, H. M. (2006). Pax2/5/8 proteins promote cell survival in C. elegans. Development, 133, 4193–4202. , & Xue, D. (2001). Mitochondrial endonuclease G is important for apoptosis in C. elegans. Nature, 412, 90–94. , & Xue, D. (2000). Demonstration of the in vivo interaction of key cell death regulators by structure-based design of second-site suppressors.

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