PMID- 2714648 OWN - NLM STAT- MEDLINE DCOM- 19890622 LR - 20190516 IS - 0890-9369 (Print) IS - 0890-9369 (Linking) VI - 3 IP - 2 DP - 1989 Feb TI - Genetic dissection of Drosophila myofibril formation: effects of actin and myosin heavy chain null alleles. PG - 131-40 AB - We used null mutations of Drosophila actin and myosin genes to investigate two aspects of myofibril assembly. First, we eliminated all actin or myosin in flight muscles to evaluate contributions of thick and thin filaments to sarcomere formation. Results demonstrate that thick and thin filament arrays can assemble independently but that both are essential for sarcomeric order and periodicity. Second, we examined how filament stoichiometry affects myofibril assembly. We find that heterozygotes for actin (Act88F) or myosin heavy chain (Mhc36B) null alleles have complex myofibrillar defects, whereas Mhc36B-/+; Act88F-/+ double heterozygotes have nearly normal myofibrils. These results imply that most defects observed in single heterozygotes are due to filament imbalances, not deficits, and suggest that thick and thin filament interactions regulate myofibrillar growth and alignment. FAU - Beall, C J AU - Beall CJ AD - Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218. FAU - Sepanski, M A AU - Sepanski MA FAU - Fyrberg, E A AU - Fyrberg EA LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Genes Dev JT - Genes & development JID - 8711660 RN - 0 (Actins) RN - EC 3.6.4.1 (Myosins) SB - IM MH - Actins/biosynthesis/*genetics/physiology MH - Alleles MH - Animals MH - Drosophila/*genetics/growth & development MH - Heterozygote MH - Mutation MH - Myofibrils/*ultrastructure MH - Myosins/biosynthesis/*genetics/physiology MH - Wings, Animal/anatomy & histology EDAT- 1989/02/01 00:00 MHDA- 1989/02/01 00:01 CRDT- 1989/02/01 00:00 PHST- 1989/02/01 00:00 [pubmed] PHST- 1989/02/01 00:01 [medline] PHST- 1989/02/01 00:00 [entrez] AID - 10.1101/gad.3.2.131 [doi] PST - ppublish SO - Genes Dev. 1989 Feb;3(2):131-40. doi: 10.1101/gad.3.2.131.