|Feature type||allele||Associated gene||Dmel\Mmp1|
|Also Known As||Mmp1Q112*, Mmp1Q112|
|Map ( GBrowse )|
|Allele class||loss of function allele, amorphic allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
comment=Site of nucleic acid difference in mutant inferred by FlyBase based on reported amino acid change.
comment=The current annotation uses an upstream AUG 29aa upstream relative to previous reports. This accounts for the discrepency in the reported vs. annotated amino acid coordinate of the mutation.
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: Q112@.
|Phenotype Manifest In|
Mmp1/Mmp1[Q112stop] mutants display a similar taenidial spacing at the early third instar stage compared to controls but a reduced intertaenidial distance compared to wild type by late third instar.
43% of Mmp1[Q112stop] mutant third instar larvae display broken tracheal dorsal trunks. None survive to pupariation. 44% of Mmp1[Q112stop]/Mmp1 transheterozygous mutant third instar larvae display broken tracheal dorsal trunks.
Most Mmp1[Q112stop] mutants die during early larval stages. Mutants that do develop to pupae show normal development of the imaginal discs, trachea, and dorsal air sac primordium.
Heterozygous leg discs which are cut and then cultured in vivo for 48 hours form a blastema, as occurs in wild-type discs, but cell division still occurs in non-blastema cells.
Some Mmp1Q112stop mutants die during the second larval instar (about 30%), the rest die during the third larval instar, which lasts several days longer than in wild-type. Most Mmp1Q112stop/Mmp12 animals survive to third instar (84%), but only 7% pupariate. All 7% undergo head eversion, but none eclose. The tracheal system phenotypes of Mmp1Q112stop/Mmp12 larvae get more severe with age: 1. First instar: in small first instars larval trachea do not have quite as much slack as those of controls. This defect is more apparent in larger first instar larvae, where the tracheal system is visibly stretched and has no slack, especially along the transverse connectives. 20% (n = 25) of have breaks in their dorsal trunks, presumably caused by overstretching. 2. Second instar: shortened dorsal trunks; the posterior spiracles have moved inward; 44% (n = 62) have visible breaks in the dorsal trunks. 3. Third instar: The tracheal system is stretched dramatically toward the anterior of the animal, with prominent tracheal breaks in 42% (n = 52) and posterior spiracles separated from the surface of the cuticle in all. Mmp1Q112stop/Mmp12 larvae are variable in size, but are always small than their wild-type siblings.
|Phenotype Manifest In|
Mmp1[Q112stop],Mmp2[W307stop] double mutant embryos show normal haemocyte migration into the tail region of the embryo.
The formation of a regeneration blastema that is seen in the proximodistal portion of the leg disc after induction of wg[Act5C.PS] expression in the early third larval instar still occurs at the normal time if the animals are also carrying Mmp1[Q112stop]/+. However, the non-blastema cells (ventral leg cells) do not undergo cell-cycle arrest in the wing disc carrying Mmp1[Q112stop]/+, in contrast to non-blastema cells in animals in which wg[Act5C.PS] expression has been induced in an otherwise wild-type background. The frequency of adults that show transdetermination (wing structures in the adult legs) after induction of wg[Act5C.PS] 72 hours after egg deposition is increased to 42% if the animals are also carrying Mmp1[Q112stop]/+.
The larval lethality due to Mmp1Q112stop/Mmp12 is enhanced by Mmp2218/Mmp2W307stop from 84% survival to 3rd instar and 7% pupariating to 54% survival to 3rd instar and 4% pupariating. The larval lethality of Mmp1Q112stop; Mmp2W307stop double homozygotes (73% survive to 2nd instar, 35% to 3rd instar, and none pupariate) is greater than for either single homozygote.
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 7 )|