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. 2020 Jun 26;9(6):1554. doi: 10.3390/cells9061554

Table 1.

Mitotic roles of transcription factors.

Name
(Organism)
Mitotic
Localization
Interacting Mitotic Proteins Loss-of-Function Mitotic Phenotype Mitotic Function (Role in Cancer)
Sak1, Fkh2 (Sp) ND ND Regulate mitotic gene transcription. Defective septation [24]. Indirect
FKHRL1/FOXO3 (h) ND ND Regulates mitotic gene transcription. Defective mitotic exit and cytokinesis [23]. Indirect (TS)
Zas1 (Sp) Chromosomes ND Regulates mitotic gene transcription. Defective chromosome condensation and segregation [25]. Indirect
ERG (h) RNA processing
bodies (PBs)
ND Degrades AURKA and AURKB mRNAs. Multipolar spindles and aberrant spindle structure [26]. Indirect (TP)
BRCA1 (h) Not relevant Not relevant Regulates transcription of multiple mitotic genes, including BUB1, BUBR1/BUB1B, AURKA, ESPL1, PTTG1, ASPM, PRC1, and PLK1 [99]. Indirect (TS)
BRCA1 (m) Not relevant Not relevant Regulates SAC gene transcription, including MAD2, BUB1, BUBR1, and ZW10 [54,100]. Indirect (TS)
BRCA1 (h) Centrosomes γ-tubulin Centrosome amplification and fragmentation [31,32,33,34,35,36,37]. DIRECT (TS)
BRCA1 (Xe) Spindle poles TPX2, NuMa, XRHAMM Morphologically abnormal spindles in BRCA1-immunodepleted Xenopus egg extracts [40]. DIRECT
ATF5 (h) Centrosomes
(mother centriole) Midbody DZ
γ-tubulin,
PCNT
Defective accumulation of PCM; centriolar fragmentation, multipolar spindles; unknown function at the midbody [44,45]. DIRECT
AKNA (m) Centrosomes
(mother centriole)
γTuRC, EB1, DCTN1 Defective centrosome-driven MT regrowth after MT depolymerization [49]. DIRECT
YB-1/YBX1 (h) Centrosomes
Spindle poles
γ-tubulin, PCNT Structurally abnormal centrosomes with reduced MT nucleation ability [50,51]. DIRECT (TP)
OCT1/POU2F1 (h)
Interacts with BRCA1
Centrosomes
Kinetochores Midbody DZ
PARP-1,
APC1
Abnormal mitosis; unknown function at the midbody [52,53,54,55]. DIRECT (TP)
Oct1 (Xe) ND ND Morphologically abnormal spindles in Oct1-immunodepleted Xenopus egg extracts [52]. DIRECT
Nubbin (Dm)
(OCT1 ortholog)
Central spindle
Midbody FR
ND Unknown function at the midbody [56]. P-direct ND
p53/TP53 (h) Centrosomes ND Centrosome amplification and fragmentation [60,61,65,66,67]. P-direct (TS)
p53 (m) Centrosomes ND Centrosome amplification [58,62,63,64]. P-direct
SP1 (h) Centrosomes ND Centrosome amplification and decreased centrosome-driven MT nucleation [68]. P-direct (TP)
SP1 (m) Centrosomes ND Centrosome amplification and decreased centrosome-driven MT nucleation [68]. P-direct
SF-1/NR5A1 (m) Centrosomes ND Centrosome amplification [69,70]. P-direct
Kaiso/ZBTB33 (h) Centrosomes
Spindle
Central spindle
Midbody FR
γ-tubulin,
PCNT
No obvious mitotic defects [71,72]. P-direct MR (TS)
CTCF (h)
Interacts with Kaiso
Centrosomes
Spindle poles
Midbody DZ
ND Mitotic phenotype not investigated [73,74]. P-direct ND (TS)
SNAP45/SNAPC2 (h) Centrosomes
Spindle poles
Midbody FR
ND Multiple mitotic defects; defective chromosome condensation [75]. P-direct
ELK1 (h) Centrosomes
Spindle
Central spindle
Midbody FR
AURKA No obvious mitotic defects [20,76]. P-direct MR (TP, TS)
RUNX1 (h) Not relevant Not relevant Regulates transcription of BUBR1, BUB1, and NEK6 [78]. Indirect (TP)
RUNX1, RUNX2, RUNX3 (h) Centrosomes
Spindle
Midbody FR
γ-tubulin,
rootletin
Reduced cyclin B1 accumulation and delayed mitotic entry. No specific mitotic defects [79,80]. P-direct MR (TP)
CBFβ/CBFB (h)
Binds RUNX proteins
Midbody FR MRLC3 Defective midbody structure and cytokinesis (abscission); polyploid cells [88]. DIRECT (TS, TP)
YAP/YAP1 (h)
Binds RUNX proteins
Midbody DZ PATJ Defective cytokinesis (abscission) [90]. DIRECT (TS, TP)
Aire (m)
(AIRE in humans)
Spindle
Central spindle
AURKB, CEP55, CNTROB, HAUS5, HAUS8, CLASP1, CLASP2 Abnormal spindle poles and centrosome amplification [94]. DIRECT
HDAC3 (h)
(in complex with NCOR1, TBL1X and TBL1XR1)
Spindle ND Morphologically abnormal spindles and chromosome misalignment [96]. P-direct (TP)
Egr3 (m) Meiotic spindles of mouse females ND Meiotic phenotype not investigated [97]. P-direct ND
TFIIB (m)
(GTF2B in humans)
Meiotic spindles of mouse females ND Morphologically abnormal spindles and chromosomes misalignment after antibody injection [98]. P-direct
WT1 (h) Kinetochores
(colocalizes with MAD2)
MAD2 Accelerated metaphase-to-anaphase transition; defective chromosome segregation [101,102]. DIRECT (TS, TP)
TIF1γ/TRIM33 (h) ND CDC20,
APC/C
Chromosome misalignment; delay in metaphase-to-anaphase transition [103,104]. P-direct (TS, TP)
XPB/ERCC3 (h)
(TFIIH subunit)
Centrosomes
Spindle poles
γ-tubulin Mitotic phenotype not investigated [111]. Direct ND (TS)
Hay (Dm)
(TFIIH subunit, orthologous to XPB)
Chromosome/
spindle area in embryos
Testis-specific β2-tubulin Defective meiotic spindles in males; abnormal mitotic spindles and defective chromosome segregation in embryos from hay mutant mothers [108,109,110,113]. P-direct
p8, p52, Cdk7 (Dm)
(TFIIH subunits)
Chromosome/
spindle area in embryos
ND Abnormal mitotic spindles and defective chromosome segregation in embryos from mutant or RNAi mothers [113]. P-direct
XPD/ERCC2 (h)
(TFIIH subunit forms another complex with MIP18 and MMS19)
Spindle
(with MIP18 and MMS19)
ND Multipolar spindles and multinucleated cells [112]. P-direct
Xpd (Dm)
(TFIIH subunit)
ND Regulates Cdk7 localization Abnormal mitotic spindles and defective chromosome segregation in embryos from Xpd mutant mothers [114]. P-direct
KANSL1, KANSL3, MCRS1 (h)
(KANSL complex subunits)
Spindle poles; KANSL1 and KANSL3 bind MT minus ends TPX2,
MCAK
Chromosome misalignment and defective segregation [120,121]. DIRECT (TP)
WDR5 (h)
(KANSL subunit that forms another complex with MLL1/KMT2A)
Centrosomes Spindle
Central spindle
Midbody DZ
KIF2A,
PRC1,
MKLP1, CYK4, CEP55
Morphologically abnormal and elongated spindles, aberrant chromosome segregation, and failures in cytokinesis [124,125,126]. DIRECT (TP)
Dgt1 (Dm)
(NSL subunit orthologous to KANSL2)
Diffuse
(weak on spindle)
ND Diminished γ-tubulin at centrosomes; long spindles [17]. P-direct
Rcd1 (Dm)
(NSL subunit orthologous to KANSL3)
Centrosomes
Central spindle
Midbody FR
ND Defective centriole replication; frequent failures in chromosome alignment and segregation [18,19,127]. Indirect (P-direct MR)
Rcd5 (Dm)
(NSL subunit orthologous to MCRS1)
Centrosomes
Midbody DZ
ND Defective centriole replication; frequent failures in chromosome alignment and segregation [17,18,127]. Indirect (P-direct MR)
MBD-R2 (Dm)
(NSL subunit orthologous to PHF20)
Chromosomes ND Defective centriole replication; frequent failures in chromosome alignment and segregation [19,127]. Indirect (P-direct MR)
Wds (Dm)
(NSL subunit orthologous to WDR5)
Centrosomes
Kinetochores
Midbody DZ
ND Defective centriole replication; frequent failures in chromosome alignment and segregation [127]. Indirect (P-direct MR)

Name: Each human TF is designated either with its HUGO acronym only, or both the name used in the cited papers and the HUGO acronym. Organism: h, human; m, mouse; Dm, Drosophila melanogaster, Sp., Schizosaccharomyces pombe, Xe, Xenopus egg extracts. Mitotic localization: ND, not determined; Midbody DZ, midbody dark zone; Midbody FR, midbody flanking regions; localization to specific midbody regions has been decided based on the examination of published microphotographs. Interacting mitotic proteins: ND, not determined. Mitotic function: Indirect, controls transcription of mitotic genes; DIRECT, in addition to a role in transcription has a direct role in mitosis, namely it is a moonlighting protein that meets the 3 criteria specified in the text. P-direct, putatively direct, does not meet the 3 criteria but (in the cited papers) is thought to have a direct mitotic role. P-direct ND, localizes to a mitotic structure but its mitotic role has not been investigated. P-direct MR, localizes to a mitotic structure but its loss does not result in a detectable mitotic phenotype; it might therefore have either a minor or a redundant mitotic function. Role in cancer was determined by examination of the pertinent literature; references are not reported: TS, tumor suppressor; TP, tumor promoter; TS, TP, can function either as a tumor suppressor or promoter, depending on the cellular context.