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FB2025_05
,
released December 11, 2025
Cyc B, Cyclin B1
a G2-M phase cyclin - cell cycle regulator - dimerization partner of Cdk1/cdc2 kinase - promotes Cdk1's protein kinase activity - CycB-Cdk1 complex induces the start of mitosis - during late metaphase of mitosis and continuing in G1, CycB is rapidly degraded resulting in inactivation of Cdk1 protein kinase activity, and allowing termination of mitosis.
Please see the JBrowse view of Dmel\CycB for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.41
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.52
2.3 (unknown)
2.7 (northern blot)
2.489 (longest cDNA)
None of the polypeptides share 100% sequence identity.
64 (kD)
530 (aa); 64 (kD)
530 (aa); 65 (kD)
Interacts with the protein kinase Cdk1 to form a serine/threonine kinase holoenzyme complex also known as maturation promoting factor (MPF). The cyclin subunit imparts substrate specificity to the complex.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\CycB using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: maternally deposited
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as procephalic ectoderm primordium
Comment: reported as embryonic central brain mushroom body
CycB expression in early embryos is diffusely concentrated at the anterior end of the embryo.
High levels of CycB transcripts are observed at times of rapid cell proliferation such as early and late embryo stages and at lower levels at other times. In preblastoderm embryos, CycB transcripts are detected throughout the cytoplasm with a higher concentration at the posterior end. During nuclear migration, CycB transcripts migrate in close association with the nuclei to the periphery and the mRNA at the posterior cap is incorporated into the forming pole cells. In somatic cells, signal decreases during blastoderm stages and increases again at gastrulation, at which time, transcripts are observed throughout the embryo. During germband retraction, CycB trancripts are observed in the developing nervous system but are no longer seen in epidermal cells that have completed their cell divisions.
CycB transcripts are concentrated around nuclei in syncytial embryos and then migrate with them to the cortex. They are concentrated in the regions around nuclei that are rich in microtubules. CycB transcripts were found to be concentrated at the posterior pole of early embryos and are thought to concentrate there during oogenesis. This posterior localization was abolished in mutants of stau, vas, spir, capu, and osk. Posterior localization of CycB transcripts is less striking in tud and vls mutants than in wild type embryos and indistinguishable from wild type in nos and pum mutants. No ectopic anterior expression of CycB was seen in BicD mutants.
Post embryonic mitosis 16 CycB protein is detected primarily in the proliferating nervous system and is absent from most other embryonic tissues.
JBrowse - Visual display of RNA-Seq signals
View Dmel\CycB in JBrowse
2-101
2-105.7
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
CycB promotes germline stem cell abscission.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
CycB destruction triggers changes to kinetochore behaviour essential for successful anaphase.
CycB destruction is required for anaphase B, cytokinesis and for directional stability of univalent chromosome movements.
A deficiency of CycB causes a mitotic cycle delay at metaphase stages during blastoderm. Delay results in precocious expression of the knrl gene which compensates for partial loss of kni activity allowing kni mutant progeny to survive. Heterozygosity for CycB is sufficient for females to produce viable homozygous kni mutant progeny. Double heterozygotes for CycA and CycB increase the efficiency for kni mutant rescue suggesting the cyclins interact synergistically.
Mutations in fzy result in metaphase arrest, neither CycA, CycB or CycB3 are degraded in this arrest. Comparison of the fzy mutant phenotype with the phenotype resulting from expression of N-terminal truncated CycA, CycB or CycB3 suggests that fzy is not only required for mitotic cyclin degradation because fzy mutations, but not truncated cyclins, block chromosome separation.
During development changing levels of cell cycle regulators alters the rate limiting step and the mechanism governing progress of the cell cycle. Three phases of developmental progression of cell cycle regulation have been defined. The first seven cycles run in the presence of constitutively active cdc2. Later during cycles 8-13 increasing mitotic destruction of cyclins drives oscillations in cdc2 activity, cyclin accumulation becomes the rate limiting step for mitosis. Degradation of maternally supplied stg causes tyrosine dephosphorylation of cdc2 to become rate limiting for mitosis beginning in cycle 14.
Translation of CycB RNA in the pole cells appears to be repressed until pole cells begin proliferation in the gonad.
Maternal mRNA localises to the pole region of the embryo.
polo gene product immunoprecipitated from single Drosophila embryos can phosphorylate casein in vitro, and the kinase activity peaks cyclically at late anaphase/telophase. This contrasts with the cycling of CycB associated p34cdc2 histone H1 kinase, which is maximal upon entry into mitosis during the rapid syncitial mitoses.
As part of an investigation into the effects of 37oC heat shock on G2-phase cycle 14 embryos, the degradation of cyclin A and cyclin B in the resulting synchronised mitotic domains was shown to be delayed. 37oC heat shock applied at S phase of cycle 14 causes cell cycle arrest with microtubules in an interphase-like state, and nuclei showing unusual chromatin condensation.
Ecol\lacZ reporter gene constructs carrying the promoter of CycA and CycB have been used to identify a posterior localization sequence in CycB mRNA.
Cyclin B distribution studied in Kc line where it is detected in prophase and metaphase, localised to 2 spots, then disappears during anaphase. In an acentriolar cell line made from the maternal haploid (mh) female sterile mutant Cyclin B does not localise to 2 spots per metaphase.
CycA and CycB behaviour in syncytial embryos has been studied.
Immunocytological approach is used to address the behaviour of essential mitotic gene products in embryonic cell cycles.
CycB is not sufficient alone for mitosis. CycA and CycB are coexpressed in all proliferating cells throughout development. The regulation of CycB gene transcription is not affected by a premature stop to cell division in mutant embryos.
Two independent mechanisms act to concentrate CycB transcripts at the posterior pole of the oocyte and at the cortex of the syncytial embryo. Posterior localization of CycB transcript is disrupted in mutant embryos that fail to form pole cells.
Arrest of the cell cycle with microtubule destabilizing drugs demonstrated that CycB degradation is the key requirement for entry into anaphase.
Encodes cyclin, a molecule involved in the cell cycle; the pattern of transcription reflects this. Maternal message uniformly distributed in newly laid egg, but becomes concentrated at the posterior pole at the time of polar-nucleus migration; also evident in the cortex of the syncytial blastoderm. Larval message concentrated in the testis.
Source for identity of: CycB CG3510
