Tatiana Morozova | PubMed Health

PubMed2006

Glial and neuronal functions of the Drosophila homolog of the human SWI/SNF gene ATR-X (DATR-X) and the jing zinc-finger gene specify the lateral positioning of longitudinal glia and axons.

Neuronal-glial communication is essential for constructing the orthogonal axon scaffold in the developing Drosophila central nervous system (CNS). Longitudinal glia (LG) guide extending commissural and longitudinal axons while pioneer and commissural neurons maintain glial survival and positioning. However, the transcriptional regulatory mechanisms controlling these processes are not known. Previous studies showed that the midline function of the jing C2H2-type zinc-finger transcription factor was only partially required for axon scaffold formation in the Drosophila CNS. We therefore screened for gain-of-function enhancers of jing gain of function in the eye and identified the Drosophila homolog of the disease gene of human alpha-thalassemia/mental retardation X-linked (ATR-X) as well as other genes with potential roles in gene expression, translation, synaptic transmission, and cell cycle. jing and DATR-X reporter genes are expressed in both CNS neurons and glia, including the LG. Coexpression of jing and DATR-X in embryonic neurons synergistically affects longitudinal connective formation. During embryogenesis, jing and DATR-X have autonomous and nonautonomous roles in the lateral positioning of LG, neurons, and longitudinal axons as shown by cell-specific knockdown of gene expression. jing and DATR-X are also required autonomously for glial survival. jing and DATR-X mutations show synergistic effects during longitudinal axon formation suggesting that they are functionally related. These observations support a model in which downstream gene expression controlled by a potential DATR-X-Jing complex facilitates cellular positioning and axon guidance, ultimately allowing for proper connectivity in the developing Drosophila CNS.

Animals↗

PubMed2002

Non-cognate template usage and alternative priming by a group II intron-encoded reverse transcriptase.

Group II introns are retroelements that site-specifically insert into DNA through homing. They are also implicated in related phenomena such as ectopic site insertions and precise intron deletions, but little is known about how group II intron reverse transcriptases (RTs) interact with non-cognate substrates. Here we show that wild-type aI2 RT readily reverse transcribes non-cognate RNAs in mitochondrial RNP particles when the aI2 intron structure is misfolded. In two closely related priming mutants, 1degree2(DeltaD5) and 1(+)2(DeltaD5), which contain wild-type RT but a disrupted intron structure, the RT has substantially lost specificity for aI2 RNA and copies multiple RNAs present in the RNP particles, using an alternative priming mechanism. The RT in 1degree2(DeltaD5) RNP particles can also copy exogenous RNAs but unlike the endogenous templates, a complementary primer is required, suggesting that the alternative priming event is specific to RT-RNA interactions formed in vivo. Alternatively primed cDNAs from strains 1degree2(DeltaD5), 1(+)2(DeltaD5) and 1degree2(P714T) (containing the mutation P714T in the RT) do not use homing site DNA as a primer, but appear to utilize a non-complementary DNA primer of approximately ten nucleotides. The alternative priming mechanism and reverse transcription of non-cognate templates has implications for in vivo reverse transcription of non-intronic RNAs, which is expected to occur during intron deletions and other retroprocessing events.

DNA Primers↗