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malfunction
double isoform Gld2/Gld4 depletion results in a strong deficit in theta burst stimulation-long term potentiation and an enhancement of N-methyl-D-aspartate receptor-dependent long term depression. Gld4 depletion has negligible effects on hippocampal-dependent behaviors
malfunction
enzyme deficiency leads to reduced expression of haploid-specific mRNAs, spermiogenesis arrest and male infertility
malfunction
enzyme depletion not only reduces GLUT1 poly(A) tail length, but also GLUT1 protein. Enzyme depletion impairs glucose deprivation-induced GLUT1 up-regulation
malfunction
enzyme knock-out is lethal. Knock-down of enzyme induces apoptosis and restricts protein synthesis
malfunction
enzyme knockdown reduces mitophagosome formation
malfunction
enzyme knockout mice display reduced blood hemoglobin levels and activated primary B lymphocytes proliferate faster
malfunction
enzyme-deficient mice exhibit spermiogenesis arrest and male infertility. Enzyme loss has no impact either on the abundance of chromatoid body components such as PIWIL1, TDRD6, YBX2, and piRNAs, or on retrotransposon expression
malfunction
isoform Gld2 depletion from the mouse hippocampus results in a deficit in long term potentiation. Double isoform Gld2/Gld4 depletion results in a strong deficit in theta burst stimulation-long term potentiation and an enhancement of N-methyl-D-aspartate receptor-dependent long term depression. Gld2 depletion has negligible effects on hippocampal-dependent behaviors
malfunction
null mutations in isoform PAPS1 result in a male gametophytic defect
malfunction
reduced isoform PAPS1 activity leads to flowering-time defects
malfunction
reduced isoform PAPS4 activity leads to flowering-time defects
metabolism
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nuclear enzyme isoforms regulate transcript abundance genome-wide. Isoform Star-PAP-specific polyadenylation site usage regulates the expression of the eukaryotic translation initiation factor EIF4A1, the tumor suppressor gene PTEN and the long non-coding RNANEAT1. Isoform Star-PAP-mediated alternative polyadenylation of PTEN is essential for DNA damage-induced increase of PTEN protein levels
metabolism
the enzyme is involved in non-templated 3'-adenylation of miRNAs
physiological function
depletion of isoform Gld2 promotes rather than inhibits p53 mRNA polyadenylation/translation, induces premature senescence and enhances the stability of cytoplasmic polyadenylation element binding protein CPEB mRNA. TheCPEB 3' untranslated region contains two miR-122 binding sites, which when deleted, elevate mRNA translation. miR-122 is present in primary fibroblasts and destabilizes by Gld2 depletion
physiological function
isoform GLD4 regulates p53 polyadenylation/translation in a cytoplasmic polyadenylation element binding protein CPEB dependent manner
physiological function
knockdown of GLD2 transcripts causes male sterility, as GLD2-deficient males do not produce mature sperm. Spermatogenesis up to and including meiosis appears normal in the absence of GLD2, but post-meiotic spermatid development rapidly becomes abnormal. Nuclear bundling and F-actin assembly are defective in GLD2 knockdown testes and nuclei fail to undergo chromatin reorganization in elongated spermatids. GLD2 also affects the incorporation of protamines and the stability of dynamin and transition protein transcripts
physiological function
removal of either isoform GLD-2 or RNA-binding protein RNP-8 results in shortened poly(A) tails and lowers abundance of four target-mRNAs, i.e. oma-2, egg-1, pup-2, andtra-2. GLD-2 depletion also lowers the abundance of most GLD-2/RNP-8 putative target-mRNAs when assayed on microarrays. The GLD-2/RNP-8 complex is a broad-spectrum regulator of the oogenesis program that acts within an RNA regulatory network to specify and produce fully functional oocytes
physiological function
silencing of a few endogenous heterochromatic genes depends on isoform Cid14. The majority of these are subtelomeric genes
physiological function
a strong loss-of-function mutation in PAPS1 causes a male gametophytic defect, whereas a weak allele leads to reduced leaf growth that results in part from a constitutive pathogen response. Polyadenylation of SMALL AUXIN UP RNA (SAUR) mRNAs depends specifically on PAPS1 function. The resulting reduction in SAUR activity in PAPS1 mutants contributes to their reduced leaf growth
physiological function
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a terminal poly(A) tail is important for a subset of intron excision events that follow cleavage and polyadenylation. In these cases, splicing is promoted by the nuclear poly(A) binding protein, PABPN1, and poly(A) polymerase, PAP. Poly(A) polymerase is needed for efficient splicing. Inefficient polyadenylation is associated with impaired recruitment of splicing factors to affected introns, which are consequently degraded by the exosome
physiological function
inactivation of PAP-dependent hyperadenylation in cells leads to the upregulation of various ncRNAs, including snoRNA host genes, primary miRNA transcripts, and promoter upstream antisense RNAs. mRNAs with retained introns are susceptible to PABPN1 and PAPalpha/gamma-mediated decay. Transcripts are targeted for degradation due to inefficient export, a consequence of reduced intron number or incomplete splicing. A genetically-encoded poly(A) tail is sufficient to drive decay. Treatment with transcription inhibitors uncouples polyadenylation from decay, leading to runaway hyperadenylation of nuclear decay targets
physiological function
isoform PAPS1 plays a role in the connection between organ identity and growth patterns. Overgrowth of PAPS1 mutant petals is due to increased recruitment of founder cells into early organ primordia. The leaf phenotype of PAPS1 mutants is dominated by a constitutive immune response that leads to increased resistance to the biotrophic oomycete Hyaloperonospora arabidopsidis and reflects activation of the salicylic acid-independent signalling pathway downstream of ENHANCED DISEASE SUSCEPTIBILITY1(EDS1)/PHYTOALEXIN DEFICIENT4 (PAD4)
physiological function
mature tRNAs, which are normally not substrates for PAP I in wild-type cells, are rapidly polyadenylated as PAP I levels increase upon overexpression, leading to dramatic reductions in the fraction of aminoacylated tRNAs, cessation of protein synthesis and cell death. The toxicity associated with PAP I is exacerbated by the absence of either RNase T and/or RNase PH. Regulation of PAP I is critical not for preventing the decay of mRNAs, but rather for maintaining normal levels of functional tRNAs and protein synthesis
physiological function
nuclear RNA-dependent ATPase Mtr4 and either the nuclear non-canonical poly(A) polymerases, Trf4 or Trf5 assemble into a Trf4/5Air1/2/Mtr4 polyadenylation complex TRAMP. Disrupting the Mtr4/Trf interaction disrupts specific TRAMP and exosome functions, including small nucleolar RNA processing. A 20 amino acid peptide, residues 98-117 in the N-terminus of Trf5 is important for TRAMP complex formation
physiological function
plants lacking both isoforms PAPS2 and PAPS4 function are viable with wild-type leaf growth
physiological function
processing of the common precursor releases an incomplete tRNATyr lacking the 3'-adenosine which has to be added before addition of the CCA end and subsequent aminoacylation. Mitochondrial poly(A) polymerase mtPAP is responsible for this A addition. Complete repair can be reconstituted in vitro with three enzymes: mtPAP frequently adds more than one A to the 3'-end of the truncated tRNA, and either the mitochondrial deadenylase PDE12 or the endonuclease RNase Z trims the oligo(A) tail to a single A before CCA addition
physiological function
the trypanosome polyadenylation complex includes homologues to all four cleavage and polyadenylation specificity factor subunits, Fip1, CstF50/64, and Symplekin. Most of these factors are essential for growth and required for both in vivo polyadenylation and trans splicing
physiological function
autophagy receptor NDP52 and the enzyme form an autophagy receptor complex, which enhances autophagic elimination of damaged mitochondria
physiological function
ectopic enzyme expression inhibits proliferation as well as colony-forming ability of breast cancer cells. By regulating the expression of BCL2-interacting killer, the enzyme induces apoptosis of breast cancer cells through the mitochondrial pathway
physiological function
enzyme-mediated translational control of GLUT1 mRNA is dependent of an RNA binding protein, CPEB1, and its binding elements in the 3_UTR. Through regulating GLUT1 level, the enzyme affects glucose uptake into cells and lactate levels. The enzyme affects glucose-dependent cellular phenotypes such as migration and invasion in glioblastoma cells
physiological function
isoform Gld2 is essential for normal synaptic efficacy at least in the dentate gyrus of the hippocampus. Isoform Gld2 controls RNA processing, particularly exon skipping
physiological function
isoform Gld4 controls RNA processing, particularly exon skipping
physiological function
isoform PAPS promotes flowering in a partially redundant manner. The enzymes act antagonistically to isoform PAPS1, which delays the transition to flowering
physiological function
isoform PAPS1 interacts with the RNA-directed DNA-methylation pathway in sporophyte and pollen development. The enzyme is essential for pollen differentiation and function. Isoform PAPS1 and RDR6 function are required for transmitting-tract development
physiological function
isoform PAPS4 promotes flowering in a partially redundant manner. The enzyme acts antagonistically to isoform PAPS1, which delays the transition to flowering. Increased expression of isoform PAPS4 is sufficient to cause premature flowering
physiological function
the enzyme acts as an onco-suppressor with the specificity for B-lymphocyte lineage from which multiple myeloma originates. The enzyme controls survival and proliferation of multiple myeloma cells
physiological function
the enzyme is essential for spermatogenesis through its adenylation activitiy
physiological function
the enzyme is indispensable for the viability of human embryonic stem cells
physiological function
the enzyme is strongly induced during activation of primary splenocytes
physiological function
the enzyme regulates gene expression and probably plays a critical role during cell differentiation. Isoform FAM46C is a causal driver of multiple myeloma
physiological function
the enzyme regulates gene expression and probably plays a critical role during cell differentiation. The enzyme gene may be involved in the development of major malignancies including lung, colorectal, hepatocellular, head and neck, urothelial, endometrial and renal papillary carcinomas and melanoma
physiological function
the enzyme regulates spermiogenesis through a pathway distinct from that mediated by chromatoid body-associated factors
physiological function
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silencing of a few endogenous heterochromatic genes depends on isoform Cid14. The majority of these are subtelomeric genes
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physiological function
Trypanosoma brucei brucei 927 / 4 GUTat10.1 / TREU927
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the trypanosome polyadenylation complex includes homologues to all four cleavage and polyadenylation specificity factor subunits, Fip1, CstF50/64, and Symplekin. Most of these factors are essential for growth and required for both in vivo polyadenylation and trans splicing
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