Loss of centrioles and polyploidization in follicle cells of Drosophila melanogaster

Mahowald, Anthony P.; Caulton, J.H.; Edwards, Meredith; Floyd, Alton D.

doi:10.1016/0014-4827(79)90167-8

Cited by 71 publications

(46 citation statements)

References 10 publications

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“…1). In contrast to naturally endoreplicating cells in which centriole duplication is arrested and the centrioles retain normal morphology (Mahowald et al, 1979), endoreplicating cells of ts discs exhibited a variety of centriole forms that suggested continued and anomalous duplication cycles. Triplet forms provide insights into the control of new daughter assembly (see below) while centriole pairs with unusually long daughters provide insights into the processes that terminate replicative growth of daughter centrioles.…”

Section: Inactivation Of Cdk1 Leads To Aberrant Centriole Duplicationmentioning

confidence: 82%

Anomalous centriole configurations are detected inDrosophilawing disc cells upon Cdk1 inactivation

Vidwans

Wong

O’Farrell

2003

Journal of Cell Science

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The centriole, organizer of the centrosome, duplicates by assembling a unique daughter identical to itself in overall organization and length. The centriole is a cylindrical structure composed of nine sets of microtubules and is thus predicted to have nine-fold symmetry. During duplication, a daughter lacking discrete microtubular organization first appears off the wall of the mother centriole. It increases in length perpendicularly away from the mother and terminates growth when it matches the length of the mother. How a unique daughter of the correct length and overall organization is assembled is unknown. Here, we describe three types of unusual centriole configurations observed in wing imaginal discs of Drosophila following inactivation of Cdk1. First, we observed centriole triplets consisting of one mother and two daughters, which suggested that centrioles have more than one potential site for the assembly of daughters. Second, we observed centriole triplets comprising a grandmother, mother and daughter, which suggested that subsequent centriole duplication cycles do not require separation of mother and daughter centrioles. Finally, we observed centriole pairs in which the daughter is longer than its mother. These findings suggest that regulatory events rather than rigid structural constraints dictate features of the stereotyped duplication program of centrioles.

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Section: Inactivation Of Cdk1 Leads To Aberrant Centriole Duplicationmentioning

confidence: 82%

Anomalous centriole configurations are detected inDrosophilawing disc cells upon Cdk1 inactivation

Vidwans

Wong

O’Farrell

2003

Journal of Cell Science

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“…Egg chambers then move down a structure called the "ovariole" as they mature through stages of oogenesis (stages 1-14) (Spradling 1993). Follicle cells proliferate by a mitotic division cycle up to stage 6, and then switch to the endocycle by stage 7, undergoing three rounds of G/S endoreduplication by stage 10A (Mahowald et al 1979;Lilly and Spradling 1996;Calvi et al 1998;Deng et al 2001;Lopez-Schier and St Johnston 2001). Thereafter, they selectively rereplicate only a few loci, resulting in amplification of gene copy number (Calvi et al 1998).…”

Section: Elevated Dup Protein Induces Rereplication In Mitotic Cyclinmentioning

confidence: 99%

Endocycling cells do not apoptose in response to DNA rereplication genotoxic stress

Mehrotra¹,

Maqbool²,

Kolpakas³

et al. 2008

Genes Dev.

130

155

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Initiation of DNA replication at origins more than once per cell cycle results in rereplication and has been implicated in cancer. Here we use Drosophila to examine the checkpoint responses to rereplication in a developmental context. We find that increased Double-parked (Dup), the Drosophila ortholog of Cdt1, results in rereplication and DNA damage. In most cells, this rereplication triggers caspase activation and apoptotic cell death mediated by both p53-dependent and -independent pathways. Elevated Dup also caused DNA damage in endocycling cells, which switch to a G/S cycle during normal development, indicating that rereplication and the endocycling DNA reduplication program are distinct processes. Unexpectedly, however, endocycling cells do not apoptose regardless of tissue type. Our combined evidence suggests that endocycling apoptosis is repressed in part because proapoptotic gene promoters are silenced. Normal endocycling cells had DNA lesions near heterochromatin, which increased after rereplication, explaining why endocycling cells must constantly repress the genotoxic apoptotic response. Our results reveal a novel regulation of apoptosis in development and new insights into the little-understood endocycle. Similar mechanisms may operate during vertebrate development, with implications for cancer predisposition in certain tissues.[Keywords: DNA replication; DNA damage; endocycle; checkpoint; apoptosis] Supplemental material is available at http://www.genesdev.org. The timely duplication of the genome during S phase of every cell division cycle requires that DNA replication initiate from thousands of origins. If too few origins initiate, replication forks can collapse, resulting in DNA damage and incomplete replication of the genome. Initiation of DNA replication from origins more than once per cell cycle, however, results in "rereplication" and subsequent DNA damage (Arias and Walter 2007). In recent years, it has become increasingly apparent that problems with DNA replication are common in premalignant cells, with subsequent checkpoint defects leading to genome instability and cancer (Dutta 2007). It remains unclear, however, whether all cells in development are equivalent with respect to their regulation of DNA replication and checkpoint responses. Here, we use Drosophila to investigate the checkpoint responses to rereplication in a developmental context. Two important steps in the cell cycle regulation of DNA replication are the assembly and activation of a prereplicative complex (pre-RC) (Sivaprasad et al. 2006). The pre-RC assembles onto origins in early G1 and is subsequently activated in S phase. During pre-RC assembly, the hexameric origin recognition complex (ORC) serves as a scaffold for origin association of Cdc6 and Cdt1, which are both required to load the hexameric minichromosome maintenance complex (MCM), the replicative helicase (Randell et al. 2006;Sivaprasad et al. 2006). Once the MCM complex is tightly bound, the origins are considered to be "licensed" and competent to initiate replic...

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“…Le processus d'endoréplication est souvent associé à une simplification du cycle cellulaire: par exemple, certaines cellules suppriment la mitose en n'exprimant pas CDK1 ou ses activateurs, cycline B, cycline A ou CDC25C. De façon intéressante, certaines cellules qui « endorépliquent » ont perdu les centrosomes [33], donnant encore plus de poids à l'hypothèse selon laquelle ces structures jouent un rôle déterminant dans le déclenchement de la mitose.…”

Section: Mécanisme D'activation Des Kinases Cycline B-cdk1unclassified

Le déclenchement de la mitose chez les eucaryotes supérieurs

Dorée

2003

Med Sci (Paris)

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Le cycle cellulaire des eucaryotes présente une alternance entre deux phases, S (synthèse) et M (mitose). La phase S est une phase de duplication: celle des chromosomes, dont l'ADN se réplique par un processus semiconservatif, permettant la production de deux chromatides qui restent associées jusqu'à la transition méta-phase-anaphase de la mitose; celle également des centrosomes, qui se dupliquent par un processus mal compris, mais radicalement différent. Au début de la phase M, les centrosomes se séparent après avoir subi un processus de maturation qui augmente leur potentiel de nucléation des microtubules. Après la rupture de l'enveloppe nucléaire (chez les eucaryotes supérieurs), les paires de chromatides condensées s'associent à un appareil mitotique largement constitué de microtubules, dont la bipolarité résulte de la séparation des centrosomes. Cet appareil assure, au cours de l'anaphase, la sé-grégation des deux chromatides d'une même paire dans l'un ou l'autre de deux territoires distincts, qui se séparent au cours du clivage de la cellule en deux cellules-filles. La phase S doit être terminée avant la ségrégation des chromatides, faute de quoi une perte d'information génétique serait observée dans les cellules-filles: la phase M ne commence donc jamais avant l'achèvement de la phase S. De fait, il s'agit là de la seule contrainte absolue exercée sur le cycle cellulaire, et dans les cellules embryonnaires de nombreux métazoaires, la phase M suit immédiatement la phase S. Dans la plupart des cellules, toutefois, on observe un délai (G2) entre la phase S et la phase M, au cours duquel se produit une série de réactions intermédiaires sur lesquelles peuvent s'exercer des freins. Ces freins peuvent être activés en réponse à des signaux extracellulaires, émis par exemple par les autres cellules du même tissu. Ils peuvent l'être également en réponse à des événements délétères se produisant dans la cellule en division (par exemple, certains dommages causés à l'ADN). Le processus qui commence par la détection de MEDECINE/SCIENCES 2003 ; 19 : 299-307

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Loss of centrioles and polyploidization in follicle cells of Drosophila melanogaster

Cited by 71 publications

References 10 publications

Anomalous centriole configurations are detected inDrosophilawing disc cells upon Cdk1 inactivation

Anomalous centriole configurations are detected inDrosophilawing disc cells upon Cdk1 inactivation

Endocycling cells do not apoptose in response to DNA rereplication genotoxic stress

Le déclenchement de la mitose chez les eucaryotes supérieurs

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