Ultrastructure of mullerian and wolffian ducts of fetal rabbit in vivo and in organ culture

Djehiche, B.; Segalen, J.; Chambon, Y

doi:10.1016/0040-8166(94)90018-3

Cited by 16 publications

(9 citation statements)

References 14 publications

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“…This leads to infertility, as the ectopic organs physically block sperm release. 107 The morphology of dying wild-type MD epithelial cells in rats, mice and rabbits, is non-apoptotic: chromatin in degenerating cells is uncondensed, and the nuclear envelope is crenellated [108][109][110] (Figure 1q). These features are reminiscent of linker cell death, suggesting that MD degeneration proceeds similarly.…”

Section: Salivary Gland Cell Death In Drosophilamentioning

confidence: 99%

Non-apoptotic cell death in animal development

Kutscher

Shaham

2017

Cell Death Differ

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Programmed cell death (PCD) is an important process in the development of multicellular organisms. Apoptosis, a form of PCD characterized morphologically by chromatin condensation, membrane blebbing, and cytoplasm compaction, and molecularly by the activation of caspase proteases, has been extensively investigated. Studies in Caenorhabditis elegans, Drosophila, mice, and the developing chick have revealed, however, that developmental PCD also occurs through other mechanisms, morphologically and molecularly distinct from apoptosis. Some non-apoptotic PCD pathways, including those regulating germ cell death in Drosophila, still appear to employ caspases. However, another prominent cell death program, linker cell-type death (LCD), is morphologically conserved, and independent of the key genes that drive apoptosis, functioning, at least in part, through the ubiquitin proteasome system. These non-apoptotic processes may serve as backup programs when caspases are inactivated or unavailable, or, more likely, as freestanding cell culling programs. Non-apoptotic PCD has been documented extensively in the developing nervous system, and during the formation of germline and somatic gonadal structures, suggesting that preservation of these mechanisms is likely under strong selective pressure. Here, we discuss our current understanding of non-apoptotic PCD in animal development, and explore possible roles for LCD and other non-apoptotic developmental pathways in vertebrates. We raise the possibility that during vertebrate development, apoptosis may not be the major PCD mechanism.

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Section: Salivary Gland Cell Death In Drosophilamentioning

confidence: 99%

Non-apoptotic cell death in animal development

Kutscher

Shaham

2017

Cell Death Differ

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“…Physiological cell death plays a vital role in many aspects of vertebrate embryonic development (Saunders, 1966;Hinchcliffe, 1981), including the removal of interdigital webs (Hammar & Mottet, 1971;Alles & Sulik, 1989;, phenotypic sex determination (Jost, 1953;Price et al, 1977;Djehiche et al, 1994), establishment of balanced numbers of pre-and postsynaptic terminals in the brain and peripheral nervous system (Cowan et al, 1984;Martin & Johnson, 1991;Oppenheim, 1991), and development of the intestinal mucosa (Harmon et al, 1984) and retina (Penfold & Provis, 1986). Although the endocrine regulation of these and other paradigms of embryonic cell death is still not completely understood (Table 1), as shown by the following examples, the extracellular signals that are known can essentially be classified into one of two categories.…”

Section: Cell Death During Embryonic Developmentmentioning

confidence: 99%

“…In the case of phenotypic sex determination, cellular degeneration is actively triggered in the Müllerian duct of a genotypic male by the presence of Müllerian inhibiting substance (MIS) secreted from the embryonic testis (Josso, 1973;Price et al, 1977;Lee & Donahoe, 1993). Removal of this duct system permits only the development of the Wolffian duct (Price et al, 1977;Djehiche et al, 1994), maintained under the influence of androgens also derived from the foetal testis (Jost, 1953), that gives rise to the seminal vesicles, vas deferens and epididymis in the post-natal male (Lee & Donahoe, 1993). A similar scenario holds true for the deletion of interdigital cells in the hands and feet during embryogenesis, a process thought to be actively initiated by the presence of retinoids acting via specific cytoplasmic receptors (Alles & Sulik, 1989;.…”

Section: Cell Death During Embryonic Developmentmentioning

confidence: 99%

Physiological cell death in endocrine‐dependent tissues: an ovarian perspective

Martimbeau

Tilly

1997

Clinical Endocrinology

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“…7,8,11,25 Autophagic cell death also has been reported to occur in adulthood of insects and vertebrates including humans; it is often associated with the elimination of (large secretory) cells during adjustment of sexual organs and ancillary tissues to seasonal reproduction. 7,8,11,26,28,31 As to pathophysiology, autophagic cell death has been associated with experimental and human neurological diseases 32 ± 35 as well as cytotoxic drug treatment. 38 In summary, without attempting to force the data, the morphological observations strongly support the concept that autophagic cell death is characterised by features different from apoptosis ( Figure 1) and which is a phenomenon of general importance occurring in a broad spectrum of (patho)physiological conditions.…”

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confidence: 99%

The autophagosomal–lysosomal compartment in programmed cell death

2001

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In the last decade a tremendous progress has been achieved in understanding the control of apoptosis by survival and death factors as well as the molecular mechanisms of preparation and execution of the cell's suicide. However, accumulating evidence suggests that programmed cell death (PCD) is not confined to apoptosis but that cells use different pathways for active self-destruction as reflected by different morphology: condensation prominent, type I or apoptosis; autophagy prominent, type II; etc. Autophagic PCD appears to be a phylogenetically old phenomenon, it may occur in physiological and disease states. Recently, distinct biochemical and molecular features have been be assigned to this type of PCD. However, autophagic and apoptotic PCD should not be considered as mutually exclusive phenomena. Rather, they appear to reflect a high degree of flexibility in a cell's response to changes of environmental conditions, both physiological or pathological. Furthermore, recent data suggest that diverse or relatively unspecific signals such as photodamage or lysosomotropic agents may be mediatd by lysosomal cysteine proteases (cathepsins) to caspases and thus, apoptosis. The present paper reviews morphological, functional and biochemical/molecular data suggesting the participation of the autophagosomal ± lysosomal compartment in programmed cell death. Cell Death and Differentiation (2001) 8, 569 ± 581.

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Ultrastructure of mullerian and wolffian ducts of fetal rabbit in vivo and in organ culture

Cited by 16 publications

References 14 publications

Non-apoptotic cell death in animal development

Non-apoptotic cell death in animal development

Physiological cell death in endocrine‐dependent tissues: an ovarian perspective

The autophagosomal–lysosomal compartment in programmed cell death

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