Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as on milliways(miliAlk) as receptor for Jeb signalling

Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as on milliways(miliAlk) as receptor for Jeb signalling
复制标题

DOI:
10.1242/dev.00972
复制
发表时间:
2004-02
期刊:
--
影响因子:
--
通讯作者:
C. Stute;K. Schimmelpfeng;R. Renkawitz-Pohl;R. Palmer;A. Holz
C. Stute;K. Schimmelpfeng;R. Renkawitz-Pohl;R. Palmer;A. Holz
中科院分区:
其他
文献类型:
--
作者:
C. Stute;K. Schimmelpfeng;R. Renkawitz-Pohl;R. Palmer;A. Holz

文献摘要

被引文献

相似文献

果蝇中肠的内脏肌由合胞体组成,并由创始成肌细胞和具有融合能力的成肌细胞融合而产生,如体肌所述。一步融合导致双核圆形中肠肌肉的形成,而多步融合过程产生纵向肌肉。肌肉融合的先决条件是在融合过程本身之前在中胚层中建立成肌细胞多样性。我们提供的证据表明,在内脏中胚层的不同细胞类型的建立过程中的Notch信号的作用,表明体细胞的创始人细胞的分离的基本机制也保存在内脏创始人细胞的决定。寻找参与不同内脏细胞类型的决定和分化的基因,我们确定了两个独立的突变导致内脏中肠肌肉的损失。在这两种突变体中,内脏肌创始人细胞缺失,内脏中胚层仅由具有融合能力的成肌细胞组成。因此,没有融合发生,导致内脏肌发生完全中断。随后对突变的表征显示,它们是果冻肚(jeb)和果蝇Alk同系物(milliways)的新等位基因。我们发现,在内脏中胚层的创始人细胞的决定过程中依赖于杰布信号通过Milliways/ALK受体。此外,我们表明,在体细胞中胚层确定相反的细胞类型,融合能力的成肌细胞,也取决于杰布和ALK,揭示不同的角色杰布信号在指定成肌细胞的多样性。这种新的机制揭示了体细胞和内脏中胚层之间的串扰,导致不仅确定不同的细胞类型,但也保持分离的中胚层组织,体细胞和内脏中胚层。
The visceral muscles of the Drosophila midgut consist of syncytia and arise by fusion of founder and fusion-competent myoblasts, as described for the somatic muscles. A single-step fusion results in the formation of binucleate circular midgut muscles, whereas a multiple-step fusion process produces the longitudinal muscles. A prerequisite for muscle fusion is the establishment of myoblast diversity in the mesoderm prior to the fusion process itself. We provide evidence for a role of Notch signalling during establishment of the different cell types in the visceral mesoderm, demonstrating that the basic mechanism underlying the segregation of somatic muscle founder cells is also conserved during visceral founder cell determination. Searching for genes involved in the determination and differentiation of the different visceral cell types, we identified two independent mutations causing loss of visceral midgut muscles. In both of these mutants visceral muscle founder cells are missing and the visceral mesoderm consists of fusion-competent myoblasts only. Thus, no fusion occurs resulting in a complete disruption of visceral myogenesis. Subsequent characterisation of the mutations revealed that they are novel alleles of jelly belly (jeb) and the Drosophila Alk homologue named milliways (miliAlk). We show that the process of founder cell determination in the visceral mesoderm depends on Jeb signalling via the Milliways/Alk receptor. Moreover, we demonstrate that in the somatic mesoderm determination of the opposite cell type, the fusion-competent myoblasts, also depends on Jeb and Alk, revealing different roles for Jeb signalling in specifying myoblast diversity. This novel mechanism uncovers a crosstalk between somatic and visceral mesoderm leading not only to the determination of different cell types but also maintains the separation of mesodermal tissues, the somatic and splanchnic mesoderm.