Alterations in ribosome biogenesis cause specific defects in C. elegans hermaphrodite gonadogenesis

Voutev, Roumen; Killian, Darrell J.; Ahn, James H.; Hubbard, E. Jane Albert

doi:10.1016/j.ydbio.2006.06.011

Cited by 52 publications

(65 citation statements)

References 69 publications

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“…The ring canals allow the transfer of cytoplasm from the nurse cells to the oocyte, a key process for egg maturation. In C. elegans, the sdad1 gene is required for normal gonadal development and regulation of the germline proliferation and differentiation (Voutev et al, 2006). The preferential expression of the genes in oocytes, together with the data gained from non-vertebrate orthologs strongly, suggests that the nup54, klhl8, and sdad1 genes may have a role in fish oogenesis.…”

Section: Most Of the Gsdf Surrounding Genes Are Co-expressed In Previmentioning

confidence: 99%

The gsdf gene locus harbors evolutionary conserved and clustered genes preferentially expressed in fish previtellogenic oocytes

Gautier¹,

Gac²,

Lareyre³

2011

Gene

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Section: Most Of the Gsdf Surrounding Genes Are Co-expressed In Previmentioning

confidence: 99%

The gsdf gene locus harbors evolutionary conserved and clustered genes preferentially expressed in fish previtellogenic oocytes

Gautier¹,

Gac²,

Lareyre³

2011

Gene

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“…The Pro phenotype can occur as a result of mutations in a number of different genes encoding proteins with unrelated functions (11)(12)(13)(14)(15)(16)(17)(18)(19), and these genes act in distinct cell types, including cells of the somatic gonad and the germ line itself. Thus, whether a common cellular and molecular basis for proximal tumor formation could be found was unclear.…”

mentioning

confidence: 99%

A “latent niche” mechanism for tumor initiation

McGovern

Voutev

Maciejowski

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Stem cells, their niches, and their relationship to cancer are under intense investigation. Because tumors and metastases acquire selfrenewing capacity, mechanisms for their establishment may involve cell-cell interactions similar to those between stem cells and stem cell niches. On the basis of our studies in Caenorhabditis elegans, we introduce the concept of a ''latent niche'' as a differentiated cell type that does not normally contact stem cells nor act as a niche but that can, under certain conditions, promote the ectopic self-renewal, proliferation, or survival of competent cells that it inappropriately contacts. Here, we show that ectopic germ-line stem cell proliferation in C. elegans is driven by a latent niche mechanism and that the molecular basis for this mechanism is inappropriate Notch activation. Furthermore, we show that continuous Notch signaling is required to maintain ectopic germ-line proliferation. We highlight the latent niche concept by distinguishing it from a normal stem cell niche, a premetastatic niche and an ectopic niche. One of the important distinguishing features of this mechanism for tumor initiation is that it could operate in the absence of genetic changes to the tumor cell or the tumor-promoting cell. We propose that a latent niche mechanism may underlie tumorigenesis and metastasis in humans.Caenorhabditis elegans ͉ Delta/Serrate/LAG-2 ͉ Notch ͉ stem cell ͉ Pro phenotype

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“…( J) Quantification of A-H. Bar, 20 mm. and White 1981;McCarter et al 1997;Killian and Hubbard 2004;Voutev et al 2006), we used mosaic analysis to determine whether METT-10 acts in the soma or the germ line to inhibit germ cell proliferative fate. We generated mosaics by taking advantage of the fact that extrachromosomal arrays are imperfectly transmitted during cell division (Yochem and Herman 2005).…”

Section: Resultsmentioning

confidence: 99%

METT-10, A Putative Methyltransferase, Inhibits Germ Cell Proliferative Fate in Caenorhabditis elegans

Dorsett

Westlund²,

Schedl

2009

Genetics

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Germ-line stem cells are unique because they either self-renew through mitosis or, at a certain frequency, switch to meiosis and produce gametes. The switch from proliferation to meiosis is tightly regulated, and aberrations in switching result in either too little or too much proliferation. To understand the genetic basis of this regulation, we characterized loss-of-function mutations and a novel tumorous allele of Caenorhabditis elegans mett-10, which encodes a conserved putative methyltransferase. We show that METT-10 is a nuclear protein that acts in the germ line to inhibit the specification of germ-cell proliferative fate. METT-10 also promotes vulva, somatic gonad, and embryo development and ensures meiotic development of those germ cells that do differentiate. In addition, phenotypic analysis of a mett-10 null allele reveals that METT-10 enables mitotic cell cycle progression. The finding that METT-10 functions to inhibit germ-cell proliferative fate, despite promoting mitotic cell cycle progression of those germ cells that do proliferate, separates the specification of proliferative fate from its execution.

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Alterations in ribosome biogenesis cause specific defects in C. elegans hermaphrodite gonadogenesis

Cited by 52 publications

References 69 publications

The gsdf gene locus harbors evolutionary conserved and clustered genes preferentially expressed in fish previtellogenic oocytes

The gsdf gene locus harbors evolutionary conserved and clustered genes preferentially expressed in fish previtellogenic oocytes

A “latent niche” mechanism for tumor initiation

METT-10, A Putative Methyltransferase, Inhibits Germ Cell Proliferative Fate in Caenorhabditis elegans

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