9bp deletion (bases 1,698-1706) in the 3' untranslated region which may affect the stability of the mRNA.
A 9bp deletion in the 3 UTR which may affect mRNA stability.
cuticle & abdomen & pharate adult
cuticle & head & pharate adult
cuticle & thorax & pharate adult
In Lim36/+ embryos less than 1% of muscles 12 and 13 fail to be innervated and less than 3% of ISNb axons leave the ventral muscle field and target the transverse nerve (TN) fascicle. In stage 16 Lim36/Df(2L)TW130 embryos, 19% of hemisegments have no transverse nerve, while 38% of hemisegments have transverse nerve fasciculation defects.
Most hemizygotes do not pupariate, remaining as second or third instar larvae up to 8 or 9 days after egg laying. A few hemizygotes do pupariate 8 to 11 days after egg laying, and these pupae generally develop into pharate adults that do not eclose. These pharate adults show a complete lack of differentiated cuticle on the abdomen, and have reduced cuticle formation on the thorax and head.
Hemizygous Lim36/Df(2L)TW130 animals do not survive to the third larval instar stage.
strong allele in which second and third instar larvae persist until days eight and nine; few survive to pharate-adult stage with incomplete sclerotization.
Lim36, vvl[+]/vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by tupisl-1/tup[+]
Lim3[+]/Lim36, vvldfr-B129 has abnormal neuroanatomy | dominant phenotype, enhanceable by tupisl-1/tup[+]
Lim36 has abnormal neuroanatomy | dominant phenotype, enhanceable by Df(2L)TE35D-19/+
Lim36 has abnormal neuroanatomy | dominant phenotype, enhanceable by vvl[+]/vvldfr-B129
Lim3[+]/Lim36 is an enhancer of abnormal neuroanatomy | dominant phenotype of vvldfr-B129
Lim3[+]/Lim36 is an enhancer of abnormal neuroanatomy | dominant phenotype of tupisl-1, vvl[+]/vvldfr-B129
Lim3[+]/Lim36 is an enhancer of abnormal neuroanatomy | dominant phenotype of tupisl-1/tup[+], vvldfr-B129
Lim36 has larval intersegmental nerve | embryonic stage 16 phenotype, enhanceable by vvl[+]/vvldfr-B129
Lim36 has larval transverse nerve | embryonic stage 16 phenotype, enhanceable by vvl[+]/vvldfr-B129
Lim36, vvl[+]/vvldfr-B129 has larval intersegmental nerve | embryonic stage 16 phenotype, enhanceable by tupisl-1/tup[+]
Lim3[+]/Lim36, vvldfr-B129 has larval intersegmental nerve | embryonic stage 16 phenotype, enhanceable by tupisl-1/tup[+]
Lim36 has larval transverse nerve | embryonic stage 16 phenotype, enhanceable by Df(2L)TE35D-19/+
Lim3[+]/Lim36 is an enhancer of larval intersegmental nerve | embryonic stage 16 phenotype of vvldfr-B129
Lim3[+]/Lim36 is an enhancer of larval intersegmental nerve | embryonic stage 16 phenotype of tupisl-1, vvl[+]/vvldfr-B129
Lim3[+]/Lim36 is an enhancer of larval transverse nerve | embryonic stage 16 phenotype of vvldfr-B129
Lim3[+]/Lim36 is an enhancer of larval intersegmental nerve | embryonic stage 16 phenotype of tupisl-1/tup[+], vvldfr-B129
In Lim36/+ embryos less than 1% of muscles 12 and 13 fail to be innervated and less than 3% of ISNb axons leave the ventral muscle field and target the transverse nerve (TN) fascicle. The expressivity of these phenotypes is enhanced to 29% and 34% respectively by vvldfr-B129/+. In tupisl-1, Lim36/+; vvldfr-B129/+ embryos, the ISNb motoneurons fail to project to and innervate their specific target muscles, including muscles 12 and 13. In stage 16 Lim36/+ Df(2L)TE35D-19/+ embryos, 17% of hemisegments have no transverse nerve, while 25.5% of hemisegments have transverse nerve fasciculation defects. In stage 16 tup1/+ Lim36/+ Df(2L)TE35D-19/+ embryos, 9.3% of hemisegments have no transverse nerve, while 36% of hemisegments have transverse nerve fasciculation defects. In stage 16 tup1/+ Lim36/+ Df(2L)TE35D-19/+ embryos, 4% of hemisegments have no transverse nerve, while 46% of hemisegments have transverse nerve fasciculation defects.
Wright.
Strong allele.