I am excited to take on this new role as Editor of Birth Defects Research with a focus on the mechanisms of birth defects and developmental disorders. I was always curious about how things worked but Developmental Biology inspired me to become a scientist. When I saw my first live chick embryo with the blood flowing and intricate structures already formed after a short time, I knew that this was the career for me.

The current research in my laboratory focuses on understanding molecular and genetic mechanisms involved in the development of neural crest cells, both in normal development and disease. Neural crest cells are a fascinating population of stem‐like cells that give rise to a diverse array of cell fates including craniofacial cartilage and bone and outflow tract in the heart (Figure 1). Currently we are focused on understanding the role of transcriptional and epigenetic regulators in cranial neural crest differentiation and signaling in neural crest migration. Because of this curiosity about how embryos develop, it seemed like a natural progression to understand how normal development can go wrong causing devastating birth defects. While still passionate about normal development, I have begun to transition to birth defect research.

Currently focused on Kabuki Syndrome and Split Hand Foot Malformation (SHFM), the lab became interested in determining how normal developmental programs are defective in these birth defects to give rise to craniofacial and limb defects. Kabuki Syndrome is linked to KDMT2D and KDM6A and we have modeled the gene function in zebrafish with knockdowns and mutants (Van Laarhoven et al., 2015 and in preparation). We have studied the role of prdm1a in zebrafish neural crest development for many years (Artinger et al., 1999; Birkholz, Killian, George, & Artinger, 2009; Hernandez‐Lagunas et al., 2005; Powell, Hernandez‐Lagunas, LaMonica, & Artinger, 2013). Collaborating with labs at Greenwood Genetics Center, we have uncovered the role of a PRDM1 in SHFM. In addition, we are also developing a biorepository on my campus for discovery‐based research on craniofacial birth defects. While there have been many positives, there have also been challenges to this transition. The biggest challenges have been writing the IRB protocol and identifying clinicians who have the interest but also the time to help collaborate on a research program. I hope to use this new role as BDR editor as a platform to help other developmental biologists make this transition. From my limited experience, I have learned that the study of the basic science of birth defects is very important to the families of affected children. This should be the driving force for our continued studies, learning how to help families and their children have peace of mind and show them that there is hope for the future in the basic understanding but also for future treatment options for birth defects.

我很高兴担任出生缺陷研究编辑的新角色，重点研究出生缺陷和发育障碍的机制。我一直对事物的运作方式感到好奇，但发育生物学启发了我成为一名科学家。当我看到我的第一个活的小鸡胚胎时，它的血液在短时间内流动并形成了复杂的结构，我知道这就是我的职业。

我实验室目前的研究重点是了解正常发育和疾病中神经嵴细胞发育所涉及的分子和遗传机制。神经嵴细胞是一种迷人的干细胞样细胞群，可产生多种细胞命运，包括颅面软骨、骨骼和心脏流出道（图 1）。目前，我们专注于了解转录和表观遗传调节因子在颅神经嵴分化和神经嵴迁移信号传导中的作用。由于对胚胎如何发育的这种好奇心，了解正常发育如何出错导致毁灭性的先天缺陷似乎是一种自然的进步。虽然仍然对正常发育充满热情，但我已经开始过渡到先天缺陷研究。

目前专注于歌舞伎综合症和手足畸形（SHFM），该实验室开始对确定正常发育程序如何在这些先天缺陷中存在缺陷而导致颅面和四肢缺陷感兴趣。Kabuki 综合征与 KDMT2D 和 KDM6A 相关，我们已经对斑马鱼的基因功能进行了基因敲除和突变建模（Van Laarhoven 等人，2015 年和准备中）。多年来，我们一直在研究prdm1a在斑马鱼神经嵴发育中的作用（Artinger 等人，1999 年；Birkholz、Killian、George 和 Artinger，2009 年；Hernandez-Lagunas 等人，2005 年；Powell、Hernandez-Lagunas、LaMonica , & Artinger, 2013）。通过与格林伍德遗传学中心的实验室合作，我们发现了 PRDM1 在 SHFM 中的作用。此外，我们还在我的校园开发一个生物库，用于基于发现的颅面先天缺陷研究。虽然有许多积极的一面，但这种转变也面临着挑战。最大的挑战是编写 IRB 协议并确定有兴趣但有时间帮助合作研究项目的临床医生。我希望以 BDR 编辑这一新角色为平台，帮助其他发育生物学家实现这一转变。从我有限的经验中，我了解到研究出生缺陷的基础科学对受影响儿童的家庭非常重要。这应该是我们继续学习的动力，