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Genes
Special Issues
Gene Regulation of Development and Evolution in Mammals
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Gene Regulation of Development and Evolution in Mammals

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Animal Genetics and Genomics".

Deadline for manuscript submissions: 25 July 2025 | Viewed by 1742

Special Issue Editors

Dr. Ming Shen

E-Mail Website
Guest Editor
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China
Interests: reproduction; endocrinology; follicular development; apoptosis signaling; autophagy; angiogenesis; redox biology; cell cycle progression; hypoxia response; epigenetics
Dr. Jiaqing Zhang

E-Mail Website
Guest Editor
Institute of Animal Husbandry and Veterinary Science, Henan Academy of Agricultural Sciences, Zhengzhou, China
Interests: follicular development; oocyte maturation; embryonic development; transgenic animal; somatic cell cloning

Special Issue Information

Dear Colleagues,

The regulation of gene expression is fundamental to mammalian development, reproduction, and evolution. In recent years, significant progress in genomics, epigenetics, and gene editing technologies has shed light on the complex networks that govern processes such as gametogenesis, fertilization, embryonic development, and the formation of species-specific traits. Understanding these molecular mechanisms not only enriches our knowledge of mammalian biology but also has far-reaching implications for reproductive medicine, evolutionary biology, and the treatment of genetic disorders.

This Special Issue invites submissions of original research articles, review articles, and communications that explore the latest advances in gene regulation related to development, evolution, and reproduction in mammals, aiming to showcase cutting-edge discoveries and emerging trends in the field.

Dr. Ming Shen
Dr. Jiaqing Zhang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • gene regulation
  • mammalian development
  • evolutionary genomics
  • epigenetics
  • transcriptional control
  • developmental biology
  • gene expression networks
  • evolutionary biology
  • molecular mechanisms

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

10 pages, 1459 KiB  
Communication
MicroRNA Expression Profile Analysis in Blood During Giant Panda (Ailuropoda melanoleuca) Growth and Development
by Shanshan Ling, Die Deng, Fuxing Yang, Pingfeng Wang, Ming He, Qian Wang, Linhua Deng, Xun Wang, Ling Zhao, Gang Ye and Xiaoyu Huang
Genes 2025, 16(3), 243; https://doi.org/10.3390/genes16030243 - 20 Feb 2025
Viewed by 459
Abstract
Background/Objectives: Blood is an essential component of the immune system. As post-transcriptional regulators, miRNAs, abundant in blood, are necessary aspects in blood’s immune and physiological functions. However, there is limited knowledge about the expression and function of miRNAs in the blood of giant [...] Read more.
Background/Objectives: Blood is an essential component of the immune system. As post-transcriptional regulators, miRNAs, abundant in blood, are necessary aspects in blood’s immune and physiological functions. However, there is limited knowledge about the expression and function of miRNAs in the blood of giant pandas. Methods: We comparatively analyzed miRNA expression profiles in the blood of giant pandas of different ages using small-RNA sequencing technology. Results: We identified 393 known miRNAs, 219 conserved miRNAs, and 71 novel miRNAs in the blood of giant pandas, and functional enrichment analysis showed that the genes regulated by DE (differentially expressed) miRNAs were mainly enriched in the regulation of enzyme-linked receptor protein signaling pathways and the signaling pathways of MAPK, Hippo, and FoXO. Conclusions: Our study clarified giant pandas’ blood miRNA expression profiles at different developmental stages, which will help elucidate the blood immunity and regulation of blood cell physiological functions in giant pandas. Full article
(This article belongs to the Special Issue Gene Regulation of Development and Evolution in Mammals)
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18 pages, 13184 KiB  
Article
Lactate Promotes Hypoxic Granulosa Cells’ Autophagy by Activating the HIF-1α/BNIP3/Beclin-1 Signaling Axis
by Yitong Pan, Gang Wu, Min Chen, Xiumei Lu, Ming Shen, Hongmin Li and Honglin Liu
Genes 2025, 16(1), 14; https://doi.org/10.3390/genes16010014 - 26 Dec 2024
Viewed by 1003
Abstract
Background/Objectives: The avascular nature of the follicle creates a hypoxic microenvironment, establishing a niche where granulosa cells (GCs) rely on glycolysis to produce energy in the form of lactate (L-lactate). Autophagy, an evolutionarily conserved stress-response process, involves the formation of autophagosomes to encapsulate [...] Read more.
Background/Objectives: The avascular nature of the follicle creates a hypoxic microenvironment, establishing a niche where granulosa cells (GCs) rely on glycolysis to produce energy in the form of lactate (L-lactate). Autophagy, an evolutionarily conserved stress-response process, involves the formation of autophagosomes to encapsulate intracellular components, delivering them to lysosomes for degradation. This process plays a critical role in maintaining optimal follicular development. However, whether hypoxia regulates autophagy in GCs via lactate remains unclear. Methods: In this study, we investigated lactate-induced autophagy under hypoxia by utilizing glycolysis inhibitors or silencing related genes. Results: We observed a significant increase in autophagy in ovarian GCs under hypoxic conditions, indicated by elevated LC3II levels and reduced P62 levels. Suppressing lactate production through glycolytic inhibitors (2-DG and oxamate) or silencing lactate dehydrogenase (LDHA/LDHB) effectively reduced hypoxia-induced autophagy. Further investigation revealed that the HIF1-α/BNIP3/Beclin-1 axis is essential for lactate-induced autophagy under hypoxic conditions. Inhibiting HIF-1α activity using siRNAs or PX-478 downregulated BNIP3 expression and subsequently suppressed autophagy. Similarly, BNIP3 silencing with siRNAs repressed lactate-induced autophagy in hypoxic conditions. Mechanistically, immunoprecipitation experiments showed that BNIP3 disrupted pre-existing Bcl-2/Beclin-1 complexes by competing with Bcl-2 to form Bcl-2/BNIP3 complexes. This interaction released Beclin-1, which subsequently triggered lactate-induced autophagy under hypoxic conditions. Conclusions: These findings unveil a novel mechanism by which hypoxia regulates GC autophagy through lactate production, highlighting its potential role in sustaining follicular development under hypoxic conditions. Full article
(This article belongs to the Special Issue Gene Regulation of Development and Evolution in Mammals)
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