Gene Dmel\MR

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General Information

Symbol

Dmel\MR

Species

D. melanogaster

Name

Male recombination factor

Annotation symbol

Feature type

gene

FlyBase ID

FBgn0002792

Gene Model Status

Unannotated

Stock availability

3 publicly available

Also Known As

MRF

Genomic Location

Chromosome (arm)

Recombination map

2-54

Cytogenetic map

Sequence location

Summary Information

Automatically generated summary

See sections below for more information

The gene Male recombination factor is referred to in FlyBase by the symbol Dmel\MR (FBgn0002792). It is a gene from Drosophila melanogaster. Its molecular function is unknown. The biological processes in which it is involved are not known. 10 alleles are reported. No phenotypic data is available. It has no annotated transcripts. Gene has not been localized to the genome sequence.

User Contributed Data

Beta version, feedback welcome

Phenotypic Description from the Red Book (Lindsley & Zimm 1992)

Gene/Allele symbols may differ from current usage

MR: Male Recombination

A series of second chromosomes isolated from natural populations in diverse regions of the globe that, in crosses of MR-bearing males to laboratory-strain females, but not in the reciprocal crosses, produce dysgenic progeny. Such progeny transmit the MR chromosome at reduced levels compared with the homologous second chromosome; abnormalities in spermiogenesis including failure of individualization observed in dysgenic males account for 70% of the deficiency in recovery of MR (Matthews, 1981, Genetics 97: 95-111). Increased levels of gonial recombination observed in both sons (Hiraizumi, 1971, Proc. Nat. Acad. Sci. USA 68: 268-700) and daughters [demonstrated in c3G females by Sinclair and Green (Mol. Gen. Genet. 170: 219-24)]; mitotic crossing over in wing disks unaffected (Thompson and Woodruff, 1980, Genetica 49: 77-80). Both sons and daughters exhibit increased rates of spontaneous mutations, both lethal (Slatko and Hiraizumi, 1973, Genetics 75: 643-49) and at some but not all specific loci (e.g., Green, 1977, Proc. Nat. Acad. Sci. USA 74: 3490-93); the latter types of mutants usually unstable, undergoing further mutation either to more extreme alleles or back to wild type; increased mutation rates observed when combined with mei9 and mei41 (1981, Mutat. Res. 83: 191-200). All classes of chromosome rearrangements produced by dysgenic progeny, but with preferential points of breakage (Yannopoulos, Stamatis, Zacharopoulou, and Pelecanos, 1983, Mutat. Res. 108: 185-202); also shown in some cases to promote gonadal aplasia, especially at higher temperatures (Stamatis, Yannopoulos, and Pelecanos, 1981, Genet. Res. 38: 125-35); metaphase I of meiosis normal, but bridges and fragments observed in anaphase I and anaphase II in dysgenic males (Henderson, Woodruff and Thompson, 1973, Genetics 88: 93-107; Yannopoulos, 1978, Genet. Res. 239-47). Gross deletion of X-chromosome material induced by MR shown to involve an array of breakpoints, which, by in situ hybridization, are free of P-element sequences; postulated to arise through illegimate mitotic exchange (Green, Yamamoto, and Miklos, 1987, Proc. Nat. Acad. Sci. USA 84: 4533-37). The majority of the activity in several of the isolates maps to a site between Tft and pr on the left arm of chromosome two, but when that site removed residual activity remains in the genome. Mappability of the major effect to the same site in independent isolates suggests the presence of an element that is able to promote transposition but that itself is unable to transpose. Circumstantial evidence indicates that the element is P and that in addition to a functional P element, MR second chromosomes also carry defective P's. Males inheriting two doses of MR from mei-S332 fathers crossed to C(2)EN/0 females not discernably different from males with one dose; two doses of MR inherited from the mother are inactive (Green and Slatko, 1979, Mutat. Res. 62: 529-39).

            

                        geographical
    isolate                origin                ref α
    ______________________________________________________
    MR-23.5       Patras, Greece                 14, 15
    MR-31.1       Patras, Greece                   14
    MR-gb39       Sonoma County, California        3
    MR-h12        Haifa, Israel               2, 3, 4, 9
    MR-n1         Napa County, California       3, 4, 5
    MR-OK1        Oklahoma City, Oklahoma        7, 13
    MR-S90 β      Northern California              1
    MR-T007       Harlingen, Texas            6, 8, 10, 11
    MR-WO         Ohio?                            12
α
  1 = Bencze and Slatko, 1984, Genet. Res. 43:  149-58;
  2 = Green, 1977, Proc. Nat. Acad. Sci. USA 74:  3490-94;
  3 = Green, 1984, Biol. Zentralbl. 103:  1-8; 4 = Green and
  Shepherd, 1979, Genetics 92:  823-32; 5 = Green and Slatko,
  1979, Mutat. Res. 62:  529-31; 6 = Hiraizumi, 1971, Proc.
  Nat. Acad. Sci. USA 68:  268-70; 7 = Henderson, Woodruff,
  and Thompson, 1978, Genetics 88:  93-107; 8 = Hiraizumi,
  Slatko, Langley, and Nill, 1973, Genetics 73:  439-44;
  9 = Sinclair and Green, 1979, Molec. Gen. Genet. 170: 219-
  24; 10 = Slatko, 1978, Genetics 90:  105-24; 257-76;
  11 = Slatko and Hiraizumi, 1973, Genetics: 75:  643-49;
  12 = Waddle and Oster, 1974, J. Genet. 61:  177-83;
  13 = Woodruff and Thompson, 1977, Heredity 38:  291-307;
  14 = Yannopoulos and Pelecanos, 1977, Genet. Res. 29:  231-
  38; 15 = Yannopoulos, Stamatis, Zacharapolou, and Pelecanos,
  1983, Mutat. Res. 108:  185-202.
β
  Also carries Sd.

Recent Updates

Description

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FB2013_03

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Detailed Mapping Data

FlyBase Computed Cytological Location

Cytogenetic map

Evidence for location

Experimentally Determined Cytological Location

Cytogenetic map

Notes

References

Experimentally Determined Recombination Data

Location

2-54

(Slatko and Green, 1980)

Left of (cM)

(Slatko and Green, 1980)

Right of (cM)

amos

(Slatko and Green, 1980)

Notes

2/10 amos-pr crossovers between amos and MR.

(Slatko and Green, 1980)

Gene Model & Products

Comments on Gene Model

Transcript Data

Annotated Transcripts

Name

FlyBase ID

RefSeq ID

Length (nt)

Associated CDS (aa)

Additional Transcript Data & Comments

Reported size (kB)

Comments

External Data

Crossreferences

Polypeptide Data

Annotated Polypeptides

Name

FlyBase ID

Predicted MW (kDa)

Length (aa)

Theoretical pI

RefSeq ID

GenBank protein

Additional Polypeptide Data & Comments

Reported size (kDa)

Comments

External Data

Linkouts

Crossreferences

Sequences Consistent with the Gene Model

DDBJ /
EMBL /
GenBank

DNA sequence

Protein sequence

Name

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Mapped Features

Type

Symbol & Location

Additional Notes

References

External Data

Linkouts

Crossreferences

Expression Data

Transcript Expression

Additional Descriptive Data

Marker for

Subcellular Localization

CV Term

Polypeptide Expression

Additional Descriptive Data

Marker for

Subcellular Localization (GO Cellular Component)

CV term

Evidence

References

Expression Deduced from Reporters

High-Throughput Expression Data

Associated Tools

Reference

See Gelbart and Emmert, 2010.10.13 for analysis details and data files for all genes.

FlyAtlas Anatomy Microarray

modENCODE Anatomy RNA-Seq

modENCODE Development RNA-Seq

modENCODE Cell Lines RNA-Seq

modENCODE Treatments RNA-Seq

Expression Clusters

External Data & Images

Linkouts

Alleles & Phenotypes

Summary of Allele Phenotypes

Phenotype manifest in

Allele

Classical Alleles ( 10 )

For All Classical Alleles Show

Allele of MR	Mutagen	Stocks	Known lesion
MR¹⁰²		1	--
MR^h12	natural population	1	--
MR^T007	natural population	1	--
MR^23.5		0	--
MR^31.1	natural population	0	--
MR^gb39	natural population	0	--
MRⁿ¹	natural population	0	--
MR^OK1		0	--
MR^S90	natural population	0	--
MR^WO		0	--

Alleles Carried on Transgenic Constructs ( 0 )

For All Alleles Carried on Transgenic Constructs Show

Allele of MR	Class	Mutagen	Stocks	Known lesion

Aneuploid Aberrations

Transgenic Constructs & Insertions

Transgenic Constructs

Type of construct

Name

Expression data

Insertions

Type of insertions

Name

Expression data

Gene Ontology: Function, Process & Cellular Component ( 0 unique terms )

Terms Based on Experimental Evidence ( 0 terms )

Terms Based on Predictions or Assertions ( 0 terms )

Sequence Ontology: Class of Gene

gene

Interactions & Pathways

Summary of Physical Interactions

Summary of Genetic Interactions

Interacts with

Please look at the allele data for full details of the genetic interactions

MR allele

Gene

References

External Data

Linkouts

Orthologs

OrthoDB Orthologs (0) - based on analysis using Dmel annotation version 5.41

OrthoDB Ortholog Groups

OrthoDB orthology group searches

(Waterhouse et al., 2011, Nucleic Acids Res. 39(Database issue): D283--D288)

Drosophila inclusive ortholog search

No orthologs identified

Dipteran inclusive ortholog search

No orthologs identified

Insect inclusive ortholog search

No orthologs identified

Arthropod inclusive ortholog search

No orthologs identified

Metazoa inclusive ortholog search

No orthologs identified

Orthologs in Drosophila Species (None identified)

No orthologies identified

Orthologs in non-Drosophila Dipterans (None identified)

No non-Drosophilid orthologies identified

Orthologs in non-Dipteran Insects (None identified)

No non-Dipteran orthologies identified

Orthologs in non-Insect Arthropods (None identified)

No non-Insect Arthropod orthologies identified

Orthologs in non-Arthropod Metazoa (None identified)

No non-Arthropod Metazoa orthologies identified

Human Orthologs (0)

Gene

OMIM

HGNC

AAA Orthologs (0) based on analysis using Dmel annotation version 4.3

No orthologs identified

Stocks & Reagents

Stocks Listed in FlyBase ( 3 )

Bloomington

2353

MR^T007/CyO

Kyoto

101547

MR¹⁰²

101506

In(2L)Cy In(2R)Cy, Cy¹ cn² / MR^h12 bw^v76j61

Genomic Clones ( 0 )

cDNA Clones ( 0 )

cDNA Clones, Fully Sequenced

BDGP DGC clones

Other clones

cDNA Clones, End Sequenced (ESTs)

BDGP DGC clones

Other clones

RNAi & Array Information

Linkouts

GenomeRNAi - GenomeRNAi – A database for cell-based and in vivo RNAi phenotypes and reagents

•

44525

Antibody Information

Other Information

Discoverer

Etymology

Identification

Relationship to Other Genes

Source for database identity of

Source for database merge of

Additional comments

Other Comments

In Eurasian populations collected in 1977-1992 between 18 and 40% of second chromosomes show MR activity.

(Ivannikov et al., 1995)

A series of second chromosomes isolated from natural populations in diverse regions of the globe that, in crosses of MR-bearing males to laboratory-strain females, but not in the reciprocal crosses, produce dysgenic progeny. The majority of the activity in several of the isolates maps to a site between amos and pr on the left arm of chromosome two, but when that site removed residual activity remains in the genome. Mappability of the major effect to the same site in independent isolates suggests the presence of an element that is able to promote transposition but that itself is unable to transpose. Circumstantial evidence indicates that the element is P and that in addition to a functional P element, MR second chromosomes also carry defective P's. Males inheriting two doses of MR from mei-S332 fathers crossed to C(2)EN/0 females not discernibly different from males with one dose.

(Lindsley and Zimm, 1992)

Gross deletion of X-chromosome material induced by MR shown to involve an array of breakpoints, which, by in situ hybridization, are free of P-element sequences; postulated to arise through illegitimate mitotic exchange.

(Green et al., 1987)

All classes of chromosome rearrangements produced by dysgenic progeny, but with preferential points of breakage.

(Yannopoulos et al., 1983)

Increased mutation rates observed when combined with mei-9 and mei-41.

(Eeken and Sobels, 1981)

Such progeny transmit the MR chromosome at reduced levels compared with the homologous second chromosome; abnormalities in spermiogenesis including failure of individualization observed in dysgenic males account for 70% of the deficiency in recovery of MR.

(Matthews, 1981)

Shown in some cases to promote gonadal aplasia, especially at higher temperatures.

(Stamatis et al., 1981)

Two doses of MR inherited from the mother are inactive.

(Green and Slatko, 1979)

Increased levels of gonial recombination observed in daughters (demonstrated in c(3)G females).

(Sinclair and Green, 1979)

Mitotic crossing over in wing discs unaffected.

(Thompson et al., 1978)

Metaphase I of meiosis normal, but bridges and fragments observed in anaphase I and anaphase II in dysgenic males.

(Yannopoulos, 1978, Henderson et al., 1978)

Both sons and daughters exhibit increased rates of spontaneous mutations, both lethal and at some but not all specific loci the latter types of mutants usually unstable, undergoing further mutation either to more extreme alleles or back to wild type.

(Slatko and Hiraizumi, 1973, Green, 1977)

Increased levels of gonial recombination observed in sons.

(Hiraizumi, 1971)

External Crossreferences & Linkouts

Sequence Crossreferences

Other Crossreferences

Linkouts

GenomeRNAi - GenomeRNAi – A database for cell-based and in vivo RNAi phenotypes and reagents

•