Evidence map›Paper›PMID 10082569›Full record

ArticleMolecular and cellular biology1999

An N-terminal truncation uncouples the sex-transforming and dosage compensation functions of sex-lethal.

J L Yanowitz, G Deshpande, G Calhoun, P D Schedl

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Auto-regulatory feedback by RNA-binding proteins.Journal of molecular cell biology · 2019
    Review
  4. Article
  5. RNA (New York, N.Y.) · 2018
    Article
  6. Review
  7. Article
  8. Drosophila switch gene Sex-lethal can bypass its switch-gene target transformer to regulate aspects of female behavior.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  9. Article
  10. Article
  11. Article
  12. Hrp48 attenuates Sxl expression to allow for proper notch expression and signaling in wing development.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

J L YanowitzDepartment of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. jly@phoenix.princeton.edu
G Deshpande
G Calhoun
P D Schedl
Princeton University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Drosophila melanogaster, Sex-lethal (Sxl) controls autoregulation and sexual differentiation by alternative splicing but regulates dosage compensation by translational repression. To elucidate how Sxl functions in splicing and translational regulation, we have ectopically expressed a full-length Sxl protein (Sx.FL) and a protein lacking the N-terminal 40 amino acids (Sx-N). The Sx.FL protein recapitulates the activity of Sxl gain-of-function mutations, as it is both sex transforming and lethal in males. In contrast, the Sx-N protein unlinks the sex-transforming and male-lethal effects of Sxl. The Sx-N proteins are compromised in splicing functions required for sexual differentiation, displaying only partial autoregulatory activity and almost no sex-transforming activity. On the other hand, the Sx-N protein does retain substantial dosage compensation function and kills males almost as effectively as the Sx.FL protein. In the course of our analysis of the Sx.FL and Sx-N transgenes, we have also uncovered a novel, negative autoregulatory activity, in which Sxl proteins bind to the 3' untranslated region of Sxl mRNAs and decrease Sxl protein expression. This negative autoregulatory activity may be a homeostasis mechanism.

Indexed as

Alternative SplicingDosage Compensation, GeneticDrosophila ProteinsProtein Biosynthesis3' Untranslated RegionsAnimalsDrosophilaFemaleGene Expression RegulationMaleMutationRNA-Binding ProteinsSequence DeletionSex DifferentiationTransgenes3' Untranslated RegionsDrosophila ProteinsRNA-Binding ProteinsSxl protein, Drosophila

Identifiers

PMID10082569
PMCPMC84096
OpenAlexW2102914307

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.