Polytene chromosomes normal.
Nucleotide substitution: G939A. Amino acid replacement: D180N.
G13821303A
G939A|FBrf0127272
D177N | fl(2)d-PA; D53N | fl(2)d-PB; D53N | fl(2)d-PC; D53N | fl(2)d-PD
D180N|FBrf0127272
translation of the reference sequence results in a protein 3 amino acids shorter than the one predicted from accession GB:AJ243599 and in FBrf0127272
fl(2)d1 homozygotes are female lethal.
fl(2)d1/+ suppresses position effect variegation at the w locus caused by P{SUPor-P}KV00108.
50% of homozygous males and no homozygous females survive at 29oC. Lethality is during the larval stage (animals can survive until the third instar stage). 75% of homozygous males and 16% of homozygous females survive at 18oC. The females that survive at 18oC are sterile (males are fertile at both temperatures). The temperature sensitive period in females is the whole of development. fl(2)d1/fl(2)d2 females show temperature-sensitive lethality, and males show temperature-sensitive semi-lethality. The lethality of homozygous and fl(2)d1/fl(2)d2 females is partially suppressed by SxlM1. The semi-lethality of homozygous and fl(2)d1/fl(2)d2 males is independent of Sxl function. The lethality of SxlM1 males is partially suppressed in homozygous fl(2)d1 and fl(2)d1/fl(2)d2 flies. Partially suppresses the female germline phenotype of ovoD1rv23 flies.
Lethal in females and semi-lethal in males at 29oC, semi-lethal in females and nearly fully viable in males at 18oC. Homozygous adult females have reduced viability at both 18oC and 29oC, although females shifted to 29oC die earlier than flies kept at 18oC. Homozygous females also carrying SxlM1 have normal viability. Homozygous adult males have normal viability at both 18oC and 29oC, and have a slower developmental rate than wild-type. Homozygous females are inseminated less than wild-type females, this phenotype is suppressed by SxlM1. Homozygous males are able to inseminate females. Homozygous females developing at 18oC are sterile, with oogenesis arrested at the previtellogenic stages. This sterility is suppressed by SxlM1.
fl(2)d[+]/fl(2)d1 is a suppressor of partially lethal | dominant | female phenotype of SxlN.Hsp83.lacZ
The reduced viability of females carrying SxlN.Hsp83.T:Ecol\lacZ is completely suppressed by fl(2)d1/+.
The female progeny of fl(2)d1/+ females mated to SxlfP7B0/Y males show only 65.3% viability.
The female progeny of snfJ210/+ ; fl(2)d1/+ females mated to SxlfP7B0/Y males show only 27.6% viability.
The female progeny of snf148/+ ; fl(2)d1/+ females mated to SxlfP7B0/Y males show only 11.1% viability.
The female progeny of snfJ210/+ ; fl(2)d1/+ ; snf5MER females mated to SxlfP7B0/Y males show 16.1% viability.
The female progeny of U2af38ΔE18/fl(2)d1 females mated to SxlfP7B0/Y males show only 25.8% viability.
The amount of RNA transcribed from the dosage-compensated X-linked Sgs4 gene compared with that transcribed from the autosomal Sgs3 gene in fl(2)d1 heterozygotes and homozygotes has been measured. It shows that fl(2)d1 affects dosage compensation; it causes hypertranscription of the two X chromosomes in females.
Germline clonal analysis suggests that fl(2)d1 autonomously affects the development of the germline.
Homozygous larvae and heteroallelic larvae with fl(2)d2, reared at 25oC, have msl-1 and mle associated with numerous sites along the paired X chromosomes.