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Verfasst von:Johnston, Amal Joseph [VerfasserIn]   i
 Matveeva, Elena [VerfasserIn]   i
 Kirioukhova, Olga [VerfasserIn]   i
 Grossniklaus, Ueli [VerfasserIn]   i
 Gruissem, Wilhelm [VerfasserIn]   i
Titel:A dynamic reciprocal RBR-PRC2 regulatory circuit controls Arabidopsis gametophyte development
Verf.angabe:Amal J. Johnston, Elena Matveeva, Olga Kirioukhova, Ueli Grossniklaus, Wilhelm Gruissem
Umfang:7 S.
Fussnoten:Gesehen am 11.05.2017
Titel Quelle:Enthalten in: Current biology
Jahr Quelle:2008
Band/Heft Quelle:18(2008), 21, S. 1680-1686
ISSN Quelle:1879-0445
Abstract:Summary. Unlike animals that produce gametes upon differentiation of meiotic products, plants develop haploid male and female gametophytes that differentiate gametes such as sperm, egg and central cells, and accessory cells [1, 2]. Both gametophytes participate in double fertilization and give rise to the next sporophytic generation. Little is known about the function of cell-cycle genes in differentiation and development of gametophytes and in reproduction [1, 2]. RETINOBLASTOMA RELATED (RBR) is a plant homolog of the tumor suppressor Retinoblastoma (pRb), which is primarily known as negative regulator of the cell cycle [3]. We show that RBR is required for cell differentiation of male and female gametophytes in Arabidopsis and that loss of RBR perturbs expression levels of the evolutionarily ancient Polycomb Repressive Complex 2 (PRC2) subunits and their modifiers encoding PRC2 subunits or DNA METHYLTRANSFERASE 1 (MET1) [4-6], exemplifying convergent evolution involving theRBR-PRC2-MET1 regulatory pathways. In addition, RBR binds MET1, and maintenance of heterochromatin in central cells, a mechanism that is likely mediated by MET1 [7, 8], is impaired in the absence of RBR. Surprisingly, PRC2-specific H3K27-trimethylation activity represses paternal RBR allele, suggesting a functional role for a dynamic and reciprocal RBR-PRC2 regulatory circuit in cellular differentiation and reproductive development.
DOI:doi:10.1016/j.cub.2008.09.026
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Verlag: http://dx.doi.org/10.1016/j.cub.2008.09.026
 Kostenfrei: Verlag: http://www.sciencedirect.com/science/article/pii/S0960982208012529
 DOI: https://doi.org/10.1016/j.cub.2008.09.026
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1558535691
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