|Feature type||allele||Associated gene||Dmel\hth|
|Also Known As||hthP2, hthP2, P2, MEIS1P2|
|Allele class||loss of function allele, hypomorphic allele - genetic evidence|
|Mutagen||Delta2-3, P-element activity|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Caused by insertion|
|Phenotype Manifest In|
antennal segment 2 & leg | somatic clone
antennal segment 3 & leg | somatic clone
eye & adult head | ventral
Clones of homozygous hth[Meis1-P2] mutant neurons in the medulla display abnormal morphology. Tm1-like, rather than Mi1, neurons are found in homozygous hth[Meis1-P2] clones.
Abdominal hemisegments of hth[Meis1-P2] mutant embryos do not show an increase in glial progeny, but generate ectopic neurons in the dorsal lateral cortex suggesting homeotic transformation of NB6-4a to NB6-4t (in 7% of hemisegments).
Oenocytes fail to form in homozygous hth[Meis1-P2] mutant embryos. The peripheral nervous system is severely disrupted in hth[Meis1-P2] mutant embryos, and thoracic-like dch3 organs are observed in abdominal segments of these mutants.
The cuticles of hthMeis1-P2 embryos show severe head defects, segmental fusions and posterior-directed transformations of the abdominal segments. In the thorax, an almost completely naked epidermis with some sparse denticles replaces the rows of small denticles that are present in wild type. Transformations toward more posterior fates are evident in the first abdominal segment (A1) that takes on an A3-like identity. Denticle belt fusions are especially evident in the abdominal segments. hthMeis1-P2 clones induced in the antennal imaginal disc result in the transformation of the antenna towards a leg, containing a complete tarsus and a single proximal domain. Large hthMeis1-P2 clones in the legs result in the fusion of the proximal segments, the coxa and trochanter, with medial segments and the body wall. The resulting fused proximal domain has both bracted and unbracted bristles, suggesting it is comprised of both proximal and distal fates.
hthMeis1-P2 homozygous embryos produce cuticles with fusions or deletions of the ventral denticle belts.
Somatic clones homozygous for hthMeis1-P2 differentiate leg pattern elements that do not correspond to the position of the clones. They also form vesicles of tissue segregating from the surroundings. In the coxa, they differentiate bristles resembling those in the femur. This can be assessed because within the clone some bristles have bracts and others do not, a characteristic feature of the femur. These clones also tend to fuse with the femur, an event which is facilitated by the physical continuity between the presumptive coxa and femur regions, and suggests that the clones acquire femur identity. The transformations observed in somatic clones of hthMeis1-P2 homozygous cells in the leg are strictly cell autonomous. In the coxa, they differentiate bristles resembling those in the femur (some bristles develop bracts and others do not). These clones also tend to fuse with the femur, an event which is facilitated by the physical continuity between the presumptive coxa and femur regions, and suggests that the clones acquire femur identity.
Homozygous clones in the eye disc are rarely observed anterior to the morphogenetic furrow.
Large clones in the antenna result in transformation into leg. In 16% of cases, five distinct tarsal segments separated by four joints can be seen.
The circular outline of the joint between antennal segments 2 and 3 is lost in hthMeis1-P2 mutant adults.
Homozygous clones in the antenna give rise to a leg-like appendage which has two distinct segments; a complete tarsus (with five subsegments and a claw) and a single proximal segment. The appendage shows polarity along the proximo-distal (P-D) axis (as in wild type), with bristles and trichomes usually pointing distally and distinct bristle types being seen at different positions along the P-D axis. In the proximal segment, two to three spurs are usually seen distally (this type of bristle is normally found in the distal tibia). A single apical bristle (also normally found in the distal tibia of T2 legs) is seen in approximately 10% of proximal segments. Homozygous clones in the legs of all three segments result in legs with two segments; a single proximal segment and a complete tarsus (with five subsegments and a claw). The legs retain leg type-specific bristle patterns such as transverse row bristles in T1.
Homozygous clones in the female genitalia cause extra growths with additional vaginal teeth. Homozygous clones in the male genitalia occasionally show some abnormalities in the clasper teeth. Homozygous clones in the analia are wild type.
Normal alula and proximal or medial costa are never formed by clones of homozygous cells. When homozygous tissue is present, the sclerites, axilary cord and radius are also frequently missing or disorganised. Homozygous clones in the wing hinge grow poorly relative to their wild-type twin spots. Large homozygous clones induced during the first or second larval instar stages frequently result in the production of large overgrowths of wing blade tissue in place of the wing hinge. These overgrowths are located posteriorly, but can contain posterior (indicated by double row wing margin bristles) as well as anterior (indicated by the presence of vein 3-type sensilla campaniformia) wing tissue. All the overgrowths include an ectopic posterior wing margin, indicating the presence of a dorsal/ventral compartment boundary in the overgrown tissue. The overgrowths often contain wild-type tissue that has been induced to form wing. In contrast, clones within the wing blade are normal, and the mesonotum develops almost normally in the absence of hth+, with only minor alterations in the pattern of bristles, even when most of the tissue is mutant. In clones that delete the hinge, wing and notum tissues appear to mix. Large tissue overgrowths are seen in wing imaginal discs containing large homozygous clones. Two types of overgrowths are seen; ventral and posterior (ectopic wing pouch). The posterior overgrowths straddle the dorsal/ventral compartment boundary. Homozygous clones that are restricted to the dorsal compartment do not overgrow, but there is a lack of the folds normally found in the hinge region of the epithelium.
Somatic clones in the head, induced during larval stages, lead to ectopic eye structures in the head. the ventral head region (gena and rostral membrane) is reduced as a consequence of the production of ectopic eyes, and the maxillary palps are frequently absent or abnormal in these clones. Somatic clones in a Minute background results in ventral overgrowths of eye tissue and in the loss of ventral and dorsal head structures.
Homozygous embryos show defects in segmentation and head involution. The longitudinal tracts are reduced or missing and posterior commissures are often reduced. The spacing between the commissures is reduced, most notably in the thoracic segments, and abnormal outgrowth of multiple nerve roots is seen. The thoracic neuromeres are widened compared to wild-type.
Homozygous clones in ventral head tissue result in ectopic eye formation, some of which are at the tip of a tubular outgrowth. Clones within the compound eye or dorsal head structures do not show morphological phenotypes. The eye shape may be distorted when homozygous clones cross the eye border. Ectopic photoreceptor differentiation and local outgrowth can be seen in the eye-antenna discs of late third instar larvae bearing homozygous clones. These ectopic photoreceptors are only found in the ventral margin of the disc, and clones in the dorsal margin of the disc do not induce ectopic photoreceptor development. Homozygous clones in the second or third antennal segments result in transformation to leg-like structures, with larger clones producing a clear claw structure indicative of a distal leg. Clones in the coxa, femur or tibia often cause fusion of these leg segments, whereas clones in the tarsal segments are morphologically normal. Clones in the mesonotum and abdomen do not have significant morphological phenotypes.
Pigment is present only in the posterior third of the eye.
|Phenotype Manifest In|
Loss-of-function L heterozygous eye clones in a hth[Meis1-P2] heterozygous background results in a complete loss-of-ventral eye phenotype, as seen in L eye clones. L[rev6-3] heterozygous eye clones in a hth[Meis1-P2] heterozygous background results in no ventral eye loss and a wild-type eye phenotype.
The percentage of embryos given a mild heat shock (7 minutes at 37oC) producing severely defective cuticles (multiple fusions or deletions of denticle belts) is reduced (23% to 7%) when both parents are heterozygous for hthMeis1-P2.
Appendages in thoracic segment 2 (T2) which are composed of a AntpNs-rvC3 hthMeis1-P2 double mutant clone are leg-like along their entire proximo-distal (P-D) axis. However they have only two distinct segments along the P-D axis; a complete tarsus (with five subsegments and a claw) and a single proximal segment (which likely results from a fusion of the four proximal-most segments of a wild-type leg). The appendage shows polarity along the P-D axis (as in wild type), with bristles and trichomes usually pointing distally and distinct bristle types being seen at different positions along the P-D axis. In the proximal segment, two to three spurs are usually seen distally (this type of bristle is normally found in the distal tibia). AntpNs-rvC3 hthMeis1-P2 ScrC1 triple mutant clones result in two-segment appendages in T1 and T2.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 10 )|
(Aldaz et al., 2005, Ebner et al., 2005, Merabet et al., 2003, Azpiazu and Morata, 2002, Kobayashi et al., 2003, Ebner et al., 2003, Tang and Sun, 2002, Bessa et al., 2002, del Alamo Rodriguez et al., 2002, Chu et al., 2002, Casares and Mann, 2001, Dong et al., 2001, Estrada and Sanchez-Herrero, 2001, Casares and Mann, 2000, Henderson and Andrew, 2000, Yao et al., 1999, Abu-Shaar and Mann, 1998, Kurant et al., 1998, Noro et al., 2006, Emmons et al., 2007, Li-Kroeger et al., 2012, Grienenberger et al., 2003, Saadaoui et al., 2011, Hasegawa et al., 2011, Kannan et al., 2010)
(Sun, 1996.4.28, )
|Secondary FlyBase IDs|
|References ( 34 )|
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|Recent research papers ( 4 )|