Expression of c-kit encoded at the W locus of mice in developing embryonic germ cells and presumptive melanoblasts

Manova, Katya; Bachvarova, Rosemary F.

doi:10.1016/0012-1606(91)90233-s

Cited by 218 publications

(125 citation statements)

References 53 publications

Supporting

Mentioning

117

Contrasting

Unclassified

Order By: Relevance

“…The presence of IGF-R also at protein level was confirmed by Western blotting (data not shown). As expected (Manova & Bachvarova 1991, De Felici et al 1996, ovarian cell population enriched in oocytes obtained from 16.5 to 18.5 dpc embryos expressed increasing levels of transcripts for the KL receptor c-Kit (Fig. 7B).…”

Section: Caspase Activity In Cultured Oocytessupporting

confidence: 82%

Analysis of programmed cell death in mouse fetal oocytes

Lobascio¹,

Klinger²,

Scaldaferri³

et al. 2007

Reproduction

View full text Add to dashboard Cite

We report a short-term culture system that allows to define novel characteristic of programmed cell death (PCD) in fetal oocytes and to underscore new aspects of this process. Mouse fetal oocytes cultured in conditions allowing meiotic prophase I progression underwent apoptotic degeneration waves as revealed by TUNEL staining. TEM observations revealed recurrent atypical apoptotic morphologies characterized by the absence of chromatin margination and nuclear fragmentation; oocytes with autophagic and necrotic features were also observed. Further characterization of oocyte death evidenced DNA ladder, Annexin V binding, PARP cleavage, and usually caspase activation (namely caspase-2). In the aim to modulate the oocyte death process, we found that the addition to the culture medium of the pan-caspase inhibitors Z-VAD or caspase-2-specific inhibitor Z-VDVAD resulted in a partial and transient prevention of this process. Oocyte death was significantly reduced by the antioxidant agent NAC and partly prevented by KL and IGF-I growth factors. Finally, oocyte apoptosis was reduced by calpain inhibitor I and increased by rapamycin after prolonged culture.These results support the notion that fetal oocytes undergo degeneration mostly by apoptosis. This process is, however, often morphologically atypical and encompasses other forms of cell death including caspase-independent apoptosis and autophagia. The observation that oocyte death occurs mainly at certain stages of meiosis and can only be attenuated by typical anti-apoptotic treatments favors the notion that it is controlled at least in part by stage-specific oocyte-autonomous meiotic checkpoints and when activated is little amenable to inhibition being the oocyte able to switch back and forth among different death pathways.

show abstract

Section: Caspase Activity In Cultured Oocytessupporting

confidence: 82%

Analysis of programmed cell death in mouse fetal oocytes

Lobascio¹,

Klinger²,

Scaldaferri³

et al. 2007

Reproduction

View full text Add to dashboard Cite

show abstract

“…c-kit is known to be a protooncogene encoding a tryrosine kinase receptor in the PDGF/CSF-1 receptor family (Yarden et al 1987, Qiu et al 1988. In the mouse, since the expression of c-kit protein is found in spermatogonia, its signal is observed in all the stages throughout the period of testicular postnatal development (Manova et al 1990, Manova & Bachvarova 1991, Sorrentino et al 1991, Rossi et al 1992. In the pig, the expression of c-kit protein has also been detected in spermatogonia (Goddard et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Molecular cloning, testicular postnatal expression, and oocyte-activating potential of porcine phospholipase Cζ

Yoneda

Kashima²,

Yoshida³

et al. 2006

Reproduction

View full text Add to dashboard Cite

The molecular mechanism by which sperm triggers Ca 2C oscillation, oocyte activation, and early embryonic development has not been clarified. Recently, oocyte activation has been shown to be induced by sperm-specific phospholipase Cz (PLCz). The ability of PLCz to induce oocyte activation is highly conserved across vertebrates. In the present study, porcine PLCz cDNA was identified and the nucleotide sequence was determined. The expression pattern of porcine PLCz mRNA during the period of postnatal testicular development was shown to be similar to that of mouse PLCz. PLCz mRNA expression in the pig and mouse was detected only in the testes when the elongated spermatids had differentiated, and was detected from day 96 after birth in the pig. Histological examination of porcine testis during the period of postnatal development revealed the presence of spermatozoa from day 110 after birth. These findings suggest that the synthesis of PLCz mRNA starts when spermiogenesis is initiated. Microinjection of porcine PLCz complementary RNA into porcine oocytes demonstrated that porcine PLCz has the ability to trigger repetitive Ca 2C transients in porcine oocytes similar to that observed during fertilization. It was also found that porcine PLCz cRNA has the potential to induce oocyte activation and initiate embryonic development up to the blastocyst stage.

show abstract

“…Previous murine studies of homologous isoforms have demonstrated that Kit but not Kit A has constitutive weak autophosphorylation activity. 4 Transcripts and protein products of c-kit are expressed on mast cells, 5,6 hematopoietic stem cells, 6-10 melanocytes [11][12][13] Correspondence: DD Metcalfe, NIH/NIAID/LAD, Building 10, Room 11C205, 10 Center Drive, MSC 1881, Bethesda, MD 20892-1881, USA; Fax: 301 480-8384 Received 7 January 1997; accepted 16 October 1997 and germ cell lineages. 12,14 The c-kit receptor is known to mediate critical signals for the proliferation and maturation of these cells, [15][16][17] and recent studies have demonstrated that abnormalities of c-kit are associated with human diseases which are characterized by impaired or enhanced growth of cells expressing this receptor.…”

Section: Introductionmentioning

confidence: 99%

“…4 Transcripts and protein products of c-kit are expressed on mast cells, 5,6 hematopoietic stem cells, 6-10 melanocytes [11][12][13] Correspondence: DD Metcalfe, NIH/NIAID/LAD, Building 10, Room 11C205, 10 Center Drive, MSC 1881, Bethesda, MD 20892-1881, USA; Fax: 301 480-8384 Received 7 January 1997; accepted 16 October 1997 and germ cell lineages. 12,14 The c-kit receptor is known to mediate critical signals for the proliferation and maturation of these cells, [15][16][17] and recent studies have demonstrated that abnormalities of c-kit are associated with human diseases which are characterized by impaired or enhanced growth of cells expressing this receptor. Mutations of c-kit are involved in the hereditary disease piebaldism, which is characterized by loss of pigmentation, [18][19][20][21] while overexpression of c-kit mRNA is reported to be associated with myeloproliferative disorders and myelodysplastic syndromes (MDS).…”

Section: Introductionmentioning

confidence: 99%

Elevated expression of the proto-oncogene c-kit in patients with mastocytosis

et al. 1998

View full text Add to dashboard Cite

The stem cell factor (SCF)c-kit receptor interaction plays a critical role in the development and survival of mast cells. Several studies have also associated c-kit receptor mutations with the human diseases, mastocytosis and piebaldism. Overexpression of c-kit has been reported to be associated with myeloproliferative disorders and myelodysplastic syndromes. Using peripheral blood mononuclear cells (PBMCs) from 11 patients with indolent mastocytosis (category I), mastocytosis with an associated hematologic disorder (category II), or aggressive mastocytosis (category III); a patient with CMML unassociated with mastocytosis, and PBMCs from 13 normal subjects, we examined the level of expression of c-kit mRNA along with other c-kit isoforms to determine if overexpression of the c-kit receptor was associated with mastocytosis. Using quantitative competitive PCR, c-kit mRNA levels on average were found to be statistically elevated in the five patients with mastocytosis with an associated hematologic disorder and in the patient with aggressive mastocytosis as compared with controls, but not elevated in patients with indolent mastocytosis. The relative mRNA expression for the two c-kit isoforms was not significantly different in the mastocytosis patients compared with controls. This demonstration of the overexpression of c-kit mRNA in mastocytosis, and particularly those patients with clinical evidence of myelodysplastic syndrome, adds evidence to support the conclusion that mastocytosis, at least in some patients, is a feature of myelodysplasia; and suggests that determination of c-kit mRNA expression in PBMCs may provide an additional approach to assessing prognosis.

show abstract

Expression of c-kit encoded at the W locus of mice in developing embryonic germ cells and presumptive melanoblasts

Cited by 218 publications

References 53 publications

Analysis of programmed cell death in mouse fetal oocytes

Analysis of programmed cell death in mouse fetal oocytes

Molecular cloning, testicular postnatal expression, and oocyte-activating potential of porcine phospholipase Cζ

Elevated expression of the proto-oncogene c-kit in patients with mastocytosis

Contact Info

Product

Resources

About