l(1)TW6, DmNod
kinesin - cytoskeletal motor protein that functions during meiosis and mitosis - produces chromosome congression forces by microtubule plus end-directed motility and tip-tracking on polymerizing microtubule plus ends via association with EB1 plus end-directed motor - necessary for chromosome segregation during meiosis and for proper chromosome alignment along the meiotic spindle
Please see the JBrowse view of Dmel\nod for information on other features
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.50
2.4 (northern blot)
666 (aa); 74 (kD)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\nod 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: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
nod transcripts are detected in the germarium and in oogenesis stages S1-S3. Expression is again observed in stage S9-S12 egg chambers primarily in the nurse cell cytoplasm. By stage 12, the nurse cells have degenerated and nod transcripts are detected in the ooplasm. nod transcripts are detected throughout development with significantly higher levels in embryos and adult females than in other stages.
The 2.4kb nod transcript is present in In(1)nod-bd/Df(1)nod females.
The 2.4kb nod transcript is greatly reduced or absent in nod2/FBab0000863:Df (1)nod females. Only very faint staining is observed in ovaries from FBal0013066:nod2@ homozygous females.
JBrowse - Visual display of RNA-Seq signals
View Dmel\nod in JBrowse




Based on mapping of nodDTW.
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.
RNAi screen using dsRNA made from templates generated with primers directed against this gene results in chromosome misalignment on the metaphase spindle when assayed in S2 cells. This phenotype can be observed when the screen is performed with or without Cdc27 dsRNA.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Examination of meiotic prophase in nod mutants reveals that while heterochromatic pairing may be a component of the mechanism of homologous segregation, it is not sufficient to guarantee proper disjunction of nonexchange homologs.
nod is required for the correct segregation of the non-exchange chromosomes during meiosis, mutations result in a high level of nondisjunction of the non-exchange fourth chromosomes and achiasmate X chromosomes.
The nonmotor domain of the nod protein can mediate direct binding to DNA. During prometaphase nod protein is localized on oocyte chromosomes and is not restricted to either specific chromosomal regions or to the kinetochore. Thus motor-based chromosome-microtubule interactions are not limited to the centromere but extend along the chromosome arms, providing a molecular explanation for the polar ejection force.
An 82 amino acid residue segment of the tail of the nod protein is necessary for the localisation of the protein onto chromosomes.
Transmission of the Dp(1;f)1187 minichromosome is sensitive to the dosage of nod+. Multiple regions of Dp(1;f)1187 interact with nod+ to promote normal chromosome transmission. Most nod+ interactions are observed with regions that are not essential for centromere function.
The sequence of the nod protein has been compared with the sequences of a variety of kinesin family proteins.
nod gene product is required for nonexchange chromosomes.
nod protein is a member of the kinesin superfamily so it is proposed that the nod locus encodes a spindle motor that is required to hold distributively paired chromosomes at the metaphase plate until anaphase.
Females homozygous for nod alleles exhibit high frequencies of meiotic chromosome loss and nondisjunction at meiosis I. Most nod-induced nondisjunctional events involve nonexchange chromosomes. For example, in nod/nod females nondisjunction frequencies for the always nonexchange fourth chromosomes approaches 90% (the vast majority of gametes are nullo-4 ova), whereas nonexchange X chromosomes apparently disjoin at random. Both the frequency of exchange and the disjunction of exchange bivalents was shown to be normal in nod/nod females. Thus, with respect to its role in meiosis, the nod+ function appears to be limited to the distributive segregation system. Based on an analysis of secondary nondisjunction in noda/noda females, Carpenter concluded that the nod defect does not impair the process of partner choice within the distributive system, but rather specifically impairs the disjunctional process. Nonexchange chromosomes derived from noda/noda mothers also undergo nondisjunction and presumably loss, at meiosis II. In addition, chromosomes derived from noda/noda mothers are mitotically unstable. nod-induced mitotic chromosome loss is restricted to maternal nonexchange chromosomes and does not exert any discernible effect on meiosis in males or on mitotic chromosome stability (Baker, Carpenter and Ripoll, 1978). Although none of the existing nod alleles is lethal or female sterile, the dosage-sensitive antimorphic mutation l(1)TW6 (Wright, 1973) is argued to be allelic to nod on the basis of three lines of evidence. First, l(1)TW6/+ females display a meiotic phenotype that is virtually identical to that exhibited by noda/noda females. Second, the two loci map to the same position on the X chromosome (Wright, 1973; Baker). Third, a γ-ray induced revertant of l(1)TW6 was shown to be a recessive nod allele (New and Hawley).
Source for identity of: nod CG1763