Induction of H3.3 replacement histone mRNAs during the precommitment period of murine erythroleukemia cell differentiation

Dora B. Krimer, Genhong Cheng, Arthur I. Skoultchi

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

Differential hybridization to a cDNA library made from the mRNA of differentiating mouse erythroleukemia (MEL) cells has been used to identify sequences that are induced during the early stages of MEL cell differentiation. One of the differentially expressed genes identified encodes the H3.3 histone subtype. We show here that the three polyadenylated mRNAs produced from the H3.3B gene, as well as the single mRNA produced from the related H3.3A gene, are coordinately induced during the first few hours of MEL cell differentiation and subsequently down regulated as cells undergo terminal differentiation. Nuclear run-on transcription experiments indicate that the accumulation and decay of these mRNAs are controlled at the post-transcriptional level. Unlike the poly-adenylated mRNAs of two H1 histone genes that exhibit similar kinetics of induction and decay controlled by c-myc, induction of the H3.3 mRNAs is unaffected by deregulated expression of c-myc.

Original languageEnglish (US)
Pages (from-to)2873-2879
Number of pages7
JournalNucleic Acids Research
Volume21
Issue number12
StatePublished - 1993

Fingerprint

Cell Differentiation
Leukemia, Erythroblastic, Acute
Messenger RNA
Histones
Replacement
Proof by induction
Genes
Gene
Mouse
Decay
RNA Stability
Gene Library
Cell
Transcription
CDNA
Induction
Precommitment
Kinetics
Experiment

ASJC Scopus subject areas

  • Genetics
  • Statistics, Probability and Uncertainty
  • Applied Mathematics
  • Health, Toxicology and Mutagenesis
  • Toxicology
  • Genetics(clinical)

Cite this

Induction of H3.3 replacement histone mRNAs during the precommitment period of murine erythroleukemia cell differentiation. / Krimer, Dora B.; Cheng, Genhong; Skoultchi, Arthur I.

In: Nucleic Acids Research, Vol. 21, No. 12, 1993, p. 2873-2879.

Research output: Contribution to journalArticle

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