FlyBase Allele Report: Dmel\lin-28[Δ1]

General Information

Symbol

Dmel\lin-28^Δ1

Species

D. melanogaster

Name

FlyBase ID

FBal0317068

Feature type

allele

Associated gene

Dmel\lin-28

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

amorphic allele - genetic evidence

amorphic allele - molecular evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Chen et al., 2015)

amorphic allele - molecular evidence

(Chen et al., 2015)

Mutagen

P-element activity

(Chen et al., 2015)

Progenitor genotype

P{EP}lin-28^EP915

(Chen et al., 2015)

Cytology

Description

3687bp deletion that removes all lin-28 exons except the first exon which encodes the first 33 amino acids of lin-28 (generated by imprecise excision of the progenitor P{EP}lin-28^EP915 insertion).

(Chen et al., 2015)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Expression Data

Reporter Expression

Additional Information

Statement

Reference

Marker for

Reflects expression of

Reporter construct used in assay

Human Disease Associations

Disease Ontology (DO) Annotations

Models Based on Experimental Evidence ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates fragile X syndrome

modeled by Fmr1^Δ50M, Fmr1^KK107935

(Luhur et al., 2017)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

embryonic/larval salivary gland | pupal stage

(González-Itier et al., 2018)

intestinal stem cell | somatic clone

(Chen et al., 2015)

Detailed Description

Statement

Reference

lin-28^Δ1/lin-28^Δ1 and lin-28^Δ1/lin-28^dF30 animals start pupariation earlier and have significantly reduced pupal volume and weight compared to wild-type controls, but no change in timing of eclosion from the start of metamorphosis.

In lin-28^Δ1/lin-28^Δ1 pupae, degradation of salivary glands is significantly delayed.

(González-Itier et al., 2018)

Mutants that survive to adulthood are viable, fertile and normal in size and morphology when raised under standard laboratory conditions.

Mutant adults ingest food at normal levels.

Newly eclosed mutant adults have the same number of intestinal stem cells (ISCs) in the posterior midgut (PMG) as controls. However, in contrast to wild type, the mutant ISCs do not undergo expansion in response to feeding, and by 4 days after eclosion, the number of ISCs in the mutant PMG of fed adults is significantly lower than that of controls (this reduction persists as the flies age). The absence of ISC expansion in the mutant adults is not due to either elevated levels of apoptosis or an absence of ISC division.

The number of homozygous ISC-containing MARCM clones in the adult midgut remains constant at 5, 14 and 27 days after clone induction (clones induced 0-2 days after eclosion), in contrast to controls, where the number of ISC-containing clones increases approximately 3.2-fold over the first two weeks after clone induction. In addition, while the number of Dl-positive ISCs per clone increases in controls between 5 and 12 days after clone induction, in the mutant clones, ISC number decreases slightly over this time. Total cell number per clone increases slightly in the homozygous clones from 5 to 12 days after clone induction, but this increase is less than that seen in control clones.

Twinspot-MARCM clonal analysis indicates that in fed flies homozygous ISCs show a decrease in symmetric renewal compared to control clones, accompanied by an increase in symmetric differentiation. Midgut ISC division patterns are similar in starved mutants and controls. However, if the flies are then fed for 3 hours, the control ISCs show an approximately 25% increase in symmetric renewal divisions, while there is no change in the mutant ISC division pattern.

(Chen et al., 2015)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Suppressed by

Statement

Reference

lin-28^Δ1 has intestinal stem cell | somatic clone phenotype, suppressible by Scer\GAL4^Tub.PU/InR^UAS.Exel

(Chen et al., 2015)

NOT suppressed by

Statement

Reference

lin-28^Δ1 has intestinal stem cell | somatic clone phenotype, non-suppressible by Df(2L)let-7-C^KO2

(Chen et al., 2015)

lin-28^Δ1 has intestinal stem cell | somatic clone phenotype, non-suppressible by wg^{UAS.cHa.Tag:HA}/Scer\GAL4^Tub.PU

(Chen et al., 2015)

lin-28^Δ1 has intestinal stem cell | somatic clone phenotype, non-suppressible by yki^{UAS.EGFP,Tag:HA}/Scer\GAL4^Tub.PU

(Chen et al., 2015)

lin-28^Δ1 has intestinal stem cell | somatic clone phenotype, non-suppressible by yki^{S168A.UAS.EGFP,Tag:HA}/Scer\GAL4^Tub.PU

(Chen et al., 2015)

lin-28^Δ1 has intestinal stem cell | somatic clone phenotype, non-suppressible by Scer\GAL4^Tub.PU/Egfr^1.A887T.UAS

(Chen et al., 2015)

Additional Comments

Genetic Interactions

Statement

Reference

Homozygosity for Df(2L)let-7-C^KO2 does not suppress the reduction in total cell number per clone and reduction in number of Dl-positive intestinal stem cells per clone which is seen in MARCM clones in lin-28^Δ1 adults compared to clones in control adults 10 days after clone induction.

Expression of InR^{Scer\UAS.Exel} under the control of Scer\GAL4^tub.PU in lin-28^Δ1 clones in the adult midgut rescues the reduction in total cell number per clone and reduction in number of Dl-positive intestinal stem cells per clone in fed animals. There is also an increase in the number of mutant clones per intestine over tie which is consistent with increased symmetric renewal in the rescued animals.

The reduction in total cell number per clone and reduction in number of Dl-positive intestinal stem cells per clone seen in MARCM clones in the intestine of lin-28^Δ1 adults is not rescued by expression of any one of wg^{Scer\UAS.cHa.T:Ivir\HA1}, yki^{Scer\UAS.T:Avic\GFP-EGFP,T:Ivir\HA1}, yki^{S168A.Scer\UAS.T:Avic\GFP-EGFP,T:Ivir\HA1} or Egfr^{1.A887T.Scer\UAS} under the control of Scer\GAL4^tub.PU.