Insertion of P{lacW} in the third intron at nucleotide 153,036 of AE003734.
Insertion into the third intron, which separates coding exon 2 from coding exon 3 of the mod(mdg4) transcription unit. The insertion lies 121 bp downstream from the 3' junction of coding exon 2.
Insertion of a P-element into the third intron, 121bp downstream to the 5' splice junction.
lethal (with mod(mdg4)02)
lethal (with mod(mdg4)07)
mod(mdg4)m9/mod(mdg4)neo129 have 75% early pupal (P1-4) lethality, and 25% late pupa to pharate adult lethality (stage 12-15) and pharate adults show homeotic transformations: in males s6 (sternite of the sixth segment) has 3-7 (average 5) bristles, t7 (tergite of the seventh segment) is enlarged and bears several bristles; in females s7 bears 9-11 bristles and occasionally 3 large bristles instead of 2, bristles on s7 occasionally lose orientation, and t8 occasionally bears 1-2 bristles.
mod(mdg4)neo129/+ suppresses the variegation of lt due to In(2LR)ltG10 (seen in In(2LR)ltG10/Df(2L)lt10 animals derived from lt16/Df(2L)lt10 females), so that the percentage of pigmented Malpighian tubule cells is increased in the double mutant larvae. mod(mdg4)neo129/+ suppresses the variegation of lt due to In(2L)ltX2 (seen in In(2L)ltX2/Df(2L)lt10 animals derived from lt16/Df(2L)lt10 females), so that the percentage of pigmented Malpighian tubule cells is increased in the double mutant larvae. mod(mdg4)neo129/+ does not suppress the variegation of lt due to T(2;3)ltX13 (seen in T(2;3)ltX13/Df(2L)lt10 animals derived from lt16/Df(2L)lt10 females); there is no significant change in the percentage of pigmented Malpighian tubule.
Enhances the variegation in, i.e. reduces the eye pigmentation of, In(1)wm4h, Su(var)2-11 males. Homozygous females obtained at 29oC produce a small number of eggs that do not show signs of further development. Ovaries are of various size and ovarioles are fewer than normal and contain fewer egg chambers.
Does not enhance transinactivation of bw caused by Tp(2;2)bw-DX7.
Some homozygous escapers develop to the adult stage.
Enhances variegation of In(1)wm4h.
In(1)wm4, mod(mdg4)neo129 has enhancer of variegation phenotype, enhanceable by trxred-P6/trx[+]
mod(mdg4)neo129 has lethal | recessive phenotype, suppressible by Dvir\mod(mdg4)t11.5
mod(mdg4)neo129/mod(mdg4)02 has lethal phenotype, suppressible | partially by Dvir\mod(mdg4)t11.5
mod(mdg4)neo129/mod(mdg4)02 has lethal phenotype, suppressible | partially by Dvir\mod(mdg4)t6.8
mod(mdg4)neo129/mod(mdg4)R32 has lethal phenotype, suppressible | partially by Dvir\mod(mdg4)t11.5
mod(mdg4)07/mod(mdg4)neo129 has lethal phenotype, non-suppressible by Dvir\mod(mdg4)t11.5
mod(mdg4)neo129/mod(mdg4)[+] is an enhancer of visible | homeotic phenotype of E(var)3-41
mod(mdg4)neo129/mod(mdg4)[+] is an enhancer of enhancer of variegation phenotype of In(1)wm4, vtd2
mod(mdg4)neo129/mod(mdg4)[+] is an enhancer of visible | homeotic phenotype of trxred-P6
mod(mdg4)neo129/mod(mdg4)[+] is a suppressor of suppressor of variegation phenotype of In(1)wm4h, Su(var)2-11
mod(mdg4)neo129/mod(mdg4)ul is a non-suppressor of visible | recessive phenotype of ct6
mod(mdg4)neo129/mod(mdg4)ul is a non-suppressor of abnormal body color | recessive phenotype of y2
mod(mdg4)neo129/mod(mdg4)ul is a non-suppressor of visible | recessive phenotype of y2
In(1)wm4, mod(mdg4)neo129 has pigment cell phenotype, enhanceable by trxred-P6/trx[+]
mod(mdg4)neo129/mod(mdg4)[+] is an enhancer of adult abdominal segment 5 phenotype of E(var)3-41
mod(mdg4)neo129/mod(mdg4)[+] is an enhancer of pigment cell phenotype of In(1)wm4, vtd2
mod(mdg4)neo129/mod(mdg4)[+] is an enhancer of adult abdominal segment 5 phenotype of trxred-P6
mod(mdg4)neo129/mod(mdg4)ul is a non-suppressor of wing phenotype of ct6
mod(mdg4)neo129/mod(mdg4)ul is a non-suppressor of adult epidermis phenotype of y2
In(1)wm4h, Su(var)2-11, mod(mdg4)neo129/mod(mdg4)[+] has pigment cell phenotype
CTCFy+1 mod(mdg4)neo129 / CTCFEY15833 mod(mdg4)m9 show early pupal lethality (stage P1-4).
Enhances the homeotic transformation of A5 to A4 of trxred-P6 and E(var)3-41.
One copy of Dvir\mod(mdg4)t11.5 can rescue the lethality of mod(mdg4)neo129 homozygotes (92% of the expected progeny survive). One copy of Dvir\mod(mdg4)t11.5 can rescue the lethality of mod(mdg4)02/mod(mdg4)neo129 transheterozygotes, with the degree of rescue depending on the P{Dvir\mod(mdg4)t11.5} line used (95.1% and full viability has been seen). One copy of Dvir\mod(mdg4)t11.5 can rescue the lethality of mod(mdg4)R32/mod(mdg4)neo129 transheterozygotes. Rescued males show greater viability (63.2%) compared to rescued females (40.5%). One copy of Dvir\mod(mdg4)t11.5 does not suppresses the lethality of mod(mdg4)07/mod(mdg4)neo129 transheterozygotes. One copy of Dvir\mod(mdg4)t6.8 partially rescues the lethality of mod(mdg4)02/mod(mdg4)neo129 transheterozygotes (34% viability is seen).
mod(mdg4)neo129 is partially rescued by mod(mdg4)+t7.5
mod(mdg4)neo129 is partially rescued by mod(mdg4)t7.5
mod(mdg4)neo129 is partially rescued by mod(mdg4)+t7.5
The semi-lethal phenotype of mod(mdg4)neo129 is fully complemented by mod(mdg4)Z3-3401, but mod(mdg4)neo129 fails to complement mod(mdg4)Z3-3401 with respect to X-Y chromosome nondisjunction in male meiosis - transheterozygotes show a high level of X-Y nondisjunction (41.2%).
The lethal phenotype of mod(mdg4)neo129 is fully complemented by mod(mdg4)Z3-5578 and mod(mdg4)Z3-3298, and mod(mdg4)neo129 partially or fully complements these alleles with respect to X-Y chromosome nondisjunction in male meiosis - the transheterozygotes show only a low level of X-Y nondisjunction (frequency is indicated in parentheses after each allele); mod(mdg4)Z3-5578 (4.46%) and mod(mdg4)Z3-3298 (7.64%).
Complementation statements based on viability.
Alleles of mod(mdg4) show an allelic series for their effect on In(1)wm4h variegation. From strongest to weakest: mod(mdg4)R32 = mod(mdg4)04 = mod(mdg4)06 = mod(mdg4)07 = mod(mdg4)142Δ32 > mod(mdg4)neo129 = mod(mdg4)02 = mod(mdg4)03 > mod(mdg4)05.
Strong enhancer. High spontaneous background rate of E(var) mutations in these experiments allows for the possibility that the P insertion is not the cause of the E(var) phenotype.
P-element has been precisely excised generating wild type revertants.